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PhoenixxFire

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Biology Q&A archive/Bio FAQ
« on: April 09, 2018, 09:20:22 pm »
+35
Here's a list of all the questions previously asked in the Bio questions thread that I felt were still relevant. I've sorted it by AOS. Units 1 & 2 are all in together as there wasn't much.

Have a question that isn't answered here? You can ask it in the VCE Biology question thread

Unit 1 & 2
What do we learn in Unit 1 & 2?
Hey,
Just wanted to know what are the main concepts covered in Biology unit 1 and 2.
Just wanted to have an overview type.
Thanks
Adeena
Hey,
Welcome to AN ;D

You can read everything you'll cover here.

Basically:
-How cells work
-How things move between cells
-Photosynthesis & Cellular respiration
-How body systems work
-How we classify species
-How species interact with each other
-The cell cycle
-How organisms reproduce
-What genes and chromosomes are and what they do
-What genotypes and phenotypes are and what they're used for
-Pedigree charts and predicting offspring's genotype and phenotype
Why are genes more likely to be separated during crossing over if their loci is further apart?
Why is it that if alleles for a particular genes are further apart on a chromosomes the more likely they are to be swapped in the "crossing over" process of meiosis?
Cross overs are completely random (not true but let's assume that it is) and so the more space between genes the more chance it is that there'll be a cross over event between them.
Defining independent assortment
When defining independent assortment would it be sufficient to say: The disjunction of homologous chromosomes in anaphase 1 of meiosis is not influenced by the behavior of other pairs of homologous chromosomes.

Or would I have to include something about the alleles for genes as well, being able to separate independently into the gametes?
I'd probably just describe it as: there is an equal chance for each chromosome of each homologous pair to end up on either side of the cell equator (and thus either daughter cells) as their orientation is random. Leads to genetic variation.
Why do centromeres duplicate during meiosis?
Why do centromeres duplicate in meiosis?
In short, because you need two of them :P

The point of meiosis/mitosis is pretty much to duplicate genetic material, and you need a centromere to link sister chromatids as a component of the chromosome. Without the centromere, the genetic material cannot be compacted into the supercoiled state that is the chromosome.
Does DNA replication occur during mitosis?
Does DNA replication occur in mitosis?
no it occurs in interphase which is not part of mitosis or meiosis
When does independent assortment and segregation occur?
In Meisosis, at what stage does Independent Assortment and Segregation occur at? As in at which stage of Prophase 1, Meta 1, Ana 1, Telo 1, Prophase 2, Meta 2, Ana 2, Telo 2?

Also could someone provide good definitions for both those terms?
Independent Assortment occurs in metaphase I and Segregation occurs in anaphase I.

Segregation can be defined as the separation of paired alleles during the stage of meiosis and their independent transmission through separate gametes.
(I don't really have a definition for IA haha, even if I did it'd be informal and my interpretation)
What does hemizygous mean?
does anyone have a simple explanation of hemizygous? The definitions i found are confusing.
only one copy of the gene rather than the normal (for humans) 2
It's simply the presence of a single copy of a gene, for example the X chromosome for males (humans).

edit: Mr. T-Rav beat me to it!  :-X
What is a dihybrid cross?
Thanks for that!
Does anyone have an easy way of explaining a dihybrid cross? My book( and teacher tbh) explains it poorly.
A dihybrid cross is where the inheritance of two traits eventuate. So basically there will be two genes each with two alleles, meaning that there are now up to four possible gametes (monohybrid had two).

The new punnet square will contain 16 boxes.
Definition of complete dominance
what is a good definition for complete dominance?
Complete dominance is when the effect of one allele entirely masks the other. Thus, there are no intermediate phenotypes, unlike incomplete dominance.
What is the difference between back and test crosses?
Also what's the difference between back and test cross? What are they used for?
Back cross in when you cross an offspring with its parent or organisms that are genetically similar to its parent. Back crosses are usually done with plants.
Test cross is to cross an organism with a homozygous recessive organism. It can help identify the genotype of the organism you perform the test cross with, if it's genotype was indeed unknown.
What’s the difference between co-dominance and incomplete dominance?
difference between co dominance and incomplete dominance?
Co dominance is when both traits are expressed together equally and the full effects of both alleles is visible in the phenotype of a heterozygote. Incomplete dominance is when the partial effects of both alleles are visible in the phenotype of a heterozygote
What are the advantages of meiosis?
What are the advantages of meiosis?
The major advantage of meiosis is that it generates genetic diversity. Meiosis really is the main driver of genetic variation in humans.
How does gene linkage affect the genotype of the offspring?
How does gene linkage affect the genotype of the offspring? (What is the impact of linkage on offspring?)
If two traits are linked, they're more likely to be seen together. So if you have one chromosome that's AB and the other is ab, it's more likely that the gamete will be AB or ab rather than Ab or aB.
How can you tell if a trait is dominant or recessive?
How do you justify whether a trait is dominant or recessive, looking at a pedigree chart?
Recessive traits can skip generations, dominant traits can't.
Why do chromosomes shorten and condense during prophase?
Why do chromosomes shorten and condense during prophase?

Does this also occur in meiotic prophase I and prophase II?

Thanks!
The chromatin needs to condense so that the chromosomes can segregate appropriately - imagine how hard that'd be if it weren't condensed, with DNA basically just scattered throughout the nucleus. And yeah, it occurs in both prophase I and II (the chromatin unwinds during telophase I)
How does linkage decrease genetic variation in the offspring?
Explain how linkage decreases the amount of genetic variation in the offspring?
I'll try to answer this one as best as I can :)

Since linkage occurs as a result of genes being located very close to each other on a chromosome, the chances of one or more of the linked genes undergoing crossover is minimum. This results in a decreased amount of genetic variation in offspring.
Why does Huntington’s diseases exist given it is dominant and lethal?
Explain why Huntington disease persists in the human population when it is caused by a lethal, dominant allele.
Thanks.
Huntington's Disease does not affect individuals until they've reached a certain age (40-50), and possibly after they've had a child. It is therefore considered 'late-onset lethal'
What is a recombinant phenotype?
What is a recombinant phenotype?
A recombinant phenotype is just a phenotype that is not identical to one of the parents. So, say a long green plant is crossed with a short yellow plant and one of the offspring is short and green, it has a recombinant phenotype because none of the parents show it. The offspring that are short yellow and long green would just have parental phenotypes.
Can you tell the parents genotype from a pedigree?
can you tell from a pedigree if the parents are homozygous/heterozygous for a particular trait?
yes at times depending on the trait and offspring who have the trait - e.g. if the trait is recessive and the parents don't have the trait, and one offspring does, then the parent has to be a heterozygote for that particular trait.
Definition of independent assortment?
what is a good definition for independent assortment?
The process of random segregation and assortment of chromosomes during anaphase I of meiosis resulting in the production of genetically unique gametes.
What is meiosis?
hey guys
can someone please explain about meiosis?
the function of it
Meiosis is composed of two stages known and meiosis 1 and meiosis 2. Just to make the explanation easier, I will refer to meiosis in humans. Basically meiosis occurs in germ line cells, otherwise known as sex cells. These sex cells are diploid, so they contain 46 chromosomes or in other words 22 homologous pairs (the other two are X or Y chromosomes). These homologous chromosomes come from our parents, half from the father and half from the mother. Meiosis 1 involves the germ line cell in only one of your parents, this cell will undergo DNA replication before hand and so the 46 chromosomes will all have sister chromatids that are held together by a centromere.

(Image removed from quote.)

So as you can see in the image above, there are 46 chromosomes, but look at chromosome number 1, there are two of those, the one on the left came from the father and the one on the right came from the mother. These chromosomes are both the same, hence they are called homologous chromosomes. Before meiosis occurs, every single one of these chromosomes replicates and hence they appear as sister chromatids.

(Image removed from quote.)


Meiosis 1:
Prophase 1: The nuclear membrane disintegrates, centrosomes appear and the spindle fibre grows and chromatin condenses into chromosomes.
Metaphase 1: The homologous chromosomes all line up in the centre of the cell, along the equator. The spindle fibres attach to each homologous chromosome.
Anaphase 1: The homologous chromosomes are separated from each other, each to an opposite pole of the cell as the spindle fibres pull them apart. (for example, looking at chromosome number 1 above, there are two and because they are the same, what is the point of having them in the same new cell? Exactly, there is no point. So this helps me remember that in anaphase 1, the homologous chromosomes are separated from each other, because the cell will not benefit if it contains both of them, so one chromosome goes into cell 1 and the other goes into cell 2).
Telophase 1: Two new nuclei form around the set of chromosomes and the spindle fibres break down. The chromosomes turn into chromatin
Cytokinesis 1: The cleavage furrow moves inwards forming a region of abscission, which divides the two cells from each other.

The final result of meiosis 1 is the production of two daughter cells that both contain 23 chromosomes, where the chromosomes have sister chromatids on them.

Meiosis 2:
Prophase 2: The nuclear membranes disintegrates and spindle fibre forms as centrosomes appear. The chromatin condenses into chromosomes.
Metaphase 2: The chromosomes line up in the centre of the cell along the equator as the spindle fibres attach to the centromeres that connects the two sister chromatids.
Anaphase 2: The sister chromatids are pulled apart to opposite poles of the cell as the spindle fibres shorten. (once again, these sister chromatids are identical to each other. So why would the new cells want two chromosomes that code/instruct for the same things? Exactly, they don't need them both, so each chromatid is pulled apart to opposite cells).
Telophase 2: Two new nuclei form for each cell as the chromosomes appear as chromatin. The spindle also breaks down.
Cytokinesis 2: The cleavage furrow moves inwards which forms an abscission region that divides the two cells into four cells.

The result of meiosis 2 is four daughter cells that all have 23 chromosomes that are not composed of sister chromatids.

Now there will be four gametes formed each with only 23 chromosomes. Say for example the above was the production of four sperm cells. One of these cells will fuse with an egg cell of a female (fertilisation) and they will combine their chromosomes to a total of 46 chromosomes. This new fused cell is known as a zygote and it will undergo nuclear division (mitosis) for further development.
What’s the difference between chromosomes, chromatids, and chromatins?
Can someone explain the whole chromosome vs chromatid vs chromatin thing
Difference between chromosome and chromatin:
Alright, so DNA in our cells is always situated in the nucleus of the cell. Within the parameters of the nucleus, the DNA exists as a thin thread-like structure known as chromatin. This chromatin is the collection the all the DNA in your cells. You can imagine molecules upon molecules of chromatin, it is like a network of fibres. So, what is mitosis? The division of the nucleus, and hence how can you divide it if there is a whole structure of fibres? Exactly, these fibres, chromatin, condense (become thicker) into chromosomes during prophase of mitosis. This is done so that the nucleus can divide more readily and easily, otherwise how can you separate the network chromatin evenly into two daughter cells? So the DNA in our nucleus is only visible as chromosomes during mitosis, when it's not undergoing nuclear division, that is, not needed to divide, it exists the thread-like network, chromatin.

Difference between chromosome and chromatid:
You must understand that during the S phase of the cell cycle, the DNA in the nucleus replicates and hence the chromosomes appear as sister chromatids held together by a centromere. Each 'arm' of the chromosomal structure is known as a sister chromatid, or just simply a chromatid. The whole structure together, both the sister chromatids, is known as the chromosome. However, when the sister chromatids are separated, they are known as chromosomes and are no longer sister chromatids because they are no longer held together by that centromere.

I hope this helps xD
What level of detail do we need to know about each phase of the cell cycle?
hey guys,

what is the level of detail that we need to know for each phase of the cell cycle?
Cell cycle is composed of 5 main stages including:

- G1 phase: The cell prepares itself, grows and develops itself in size. There is a checkpoint at the end of this phase known as G0 phase or check point 1. This checkpoint ensures that the cell has appropriately grown in size and if it is ready for the next stage.

- S phase: This is the synthesis phase. The DNA of the cell replicates and hence two identical sister chromatids are present for each chromosome, held together by a centromere. (You should know the steps that occur during DNA replication)

- G2 phase: The cell further grows and develops, and new organelles are produces for the two separate cells after mitosis. There is a check point after this phase known as check point 2, and at this point the DNA replication is being checked, to ensure that all DNA has successfully replicated without any mutations.

- M phase: Mitosis phase is compose of four separate stages: Prophase, Metaphase, Anaphase, Telophase. You should also know what occurs in each of these stages. Note that there is a check point between metaphase and anaphase, to ensure that the mitotic spindle has successfully attached to the centromeres of each chromosomes, so that the sister chromatids can be pulled apart during anaphase.

- Cytokinesis: A cleavage furrow (animals) pushes inwards in the cell and a region of abscission forms, essentially dividing the two identical daughter diploid cells.

Hope that helped, that is all we need to know :)
What is a diploid organism?
What is a diploid organism?
An organism with two identical sets of chromosomes :)
What’s the purpose of finding out the F2 generation?
Can anyone explain the purpose of finding out the F2 generation?
Depends on the question. Generally to work out the alleles of the parents (by working backwards in a punnet square). Do you have a question on it?
What do you mean by working out the alleles of the parents? Is this in reference with the parent generation or F1?
I don't have a specific question on it but I really can't see why it's needed.
Either. So say you have the F1 generation and you know their phenotype but not their genotype, then by finding out the F2 generation (you wouldn't be able to predict it, the question would give you that) then you can work out the genotype of F1 (due to the percentages of different alleles in F2). You could then do the same thing again to figure out the parents genotype/phenotype now that you know the F1 generations genotypes - although I don't know why you would want to.
How many chromosomes are in the two daughter cells after telophase 1?
Can anyone explain how many chromosomes are in the two daughter cells after telophase 1?
In the first "stages" of meiosis you go from having homologous pairs to double-stranded DNA. The second  "stages" take you from doble stranded chromosomes to single stranded chromosomes (seperation of sister chromatids)


After telophase 1 you have n chromosomes in each of the two nuclei, where n is the haploid number of chromosomes (23 for humans)
But meiosis starts with a germ cell that has 46 chromosomes, then during interphase it doubles to 92 chromosomes. After all the steps of meiosis 1, telophase splits into two, so how does both daughter cells not have 46 chromosomes when the original amount was 92?
There isn't actually 92 chromosomes, there's still 46 chromosome, they just replicate so that each chromosome has a sister chromatid (the two chromatids are joined together into one chromosome - you'll probably have seen these drawn as X's. So you have two homologous chromosomes, which is a total of 4 chromtids. During meiosis one the chromosomes separate into the haploid daughter cells. Each daughter cell has one copy of each chromosome, but it has 2 chromatids which are still attached. Then during meiosis 2 the sister chromatids separate into each of the daughter cells.
What’s the symbol on a pedigree chart for a carrier?
Can anyone tell me what the symbol is for carriers on pedigree charts? Is it a dot in the middle or is it half-shaded?
Thank you!!!
Both are generally accepted. (Although, I’m speaking in general genetics and not the VCE Biology curriculum. I didn’t do VCE Biology, but I assume they’d say both too.)
What topics should I revise before going into U1 bio?
hi all, I was just wondering what concepts would be useful to revise over the holidays going into unit 1 of biology? I didn't do year 10 biology so I am a little lost in all the definitions.
Hi,
I don't think skipping year 10 biology is all that big of a deal, so don't worry about it. You do a lot of the same things in year 10 as you do in year 11 anyway, so it's not like you have missed out on anything major.
I also don't think you need to worry about revising too much over the holidays and try to enjoy them - there is plenty of time to study hard in the years ahead. But if you just like studying or are super keen to get right into the course, then by all means do. I would just recommend skimming through your textbook (if you have one) and getting a rough idea of the course and the topics. If you do come across something that's a bit difficult and you don't understand some terminology, you are more than welcome to post it here and I'm sure someone will be able to lend some help.

Good luck and I hope this helps!
If you want to have a look at some topics then learning a bit about the plasma membrane/cellular respiration/photosynthesis/mitosis/meiosis is probably your best option. But definitely wouldn't recommend learning anything in detail, you'll just end up forgetting it anyway. If you're worried just search those topics in youtube and you'll find heaps of videos explaining them :)
tbh I wouldn't go over anything in detail. Firstly because it's units 1/2 and you don't need to be too invested in it since it doesn't count towards your study score  (some aspects will flow to units 3/4 but for the most part it's only the general biology concepts that are existent in both courses). Obviously this might be a moot point if you aren't worried about scores but Also that the content assessed will vary between schools/teachers and there is no way in knowing until your teacher actually focuses on particular areas of study.

If you are just super keen to study something your best option would be to just learn whatever biology interests you to get you primed for the new year (or just do nothing and enjoy your summer holiday.
Does non-disjunction occur in the first, second, or both divisions of meiosis?
Can non-disjunction occur in the
- first OR second division of meiosis
- Both the first and second meiotic division?

I argued that it could occur in both, however my teacher says that it's the latter
Non-disjunction is both the failure of each chromosome of a homologous pair to separate in the first meiotic division, or the faluire of each sister chromatid of a chromosome to separate in the second meiotic division.
So non-disjunction can occur in both meiotic divisions  :)


Unit 1 & 2
U3 AOS 1
U3 AOS 2
U4 AOS 1
U4 AOS 1 (continued)
U4 AOS 2
U4 AOS 2 (continued)
U4 AOS 3
Detailed responses/explanations for past exam/test questions
Exam/study tips

Includes everything up to February 27th
« Last Edit: February 27, 2019, 09:56:46 am by PhoenixxFire »
2019: B Environment and Sustainability/B Science @ ANU

PhoenixxFire

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Re: Biology Q&A archive/Bio FAQ
« Reply #1 on: April 09, 2018, 09:26:27 pm »
+23
U3 AOS 1 Plasma membranes part 1
Relevant study design dot points
• the fluid mosaic model of the structure of the plasma membrane and the movement of hydrophilic and hydrophobic substances across it based on their size and polarity

• the role of different organelles including ribosomes, endoplasmic reticulum, Golgi apparatus and associated vesicles in the export of a protein product from the cell through exocytosis

• cellular engulfment of material by endocytosis.

Potato cells and Osmosis
if a potato cell is put in water why does it swell and if put it in a sugar solution, it shrinks? I know it has to do with hypotonic/hypertonic but not sure how to properly explain it.
Osmosis; free water molecules will move from a region of low solute concentration to a region of high solute concentration, across a semi permeable membrane.
If a cell is placed in a solution that is hypertonic (ie. The sugar solution) to its internal environment, then water will move out of the cell, causing it shrivel. If placed in a solution hypotonic (ie. the water) to its internal environment, then water will diffuse into the cell by osmosis. This may cause the cell to lyse.
What is the role of cholesterol in the plasma membrane?
What is the role of cholesterol in the plasma membrane?
Cholesterol's primary role is to regulate the fluidity and flexibility of the plasma membrane. This is done by preventing it from bunching up, and freezing in cold conditions. Conversely, it keeps the phospholipids closer together in cases of high temperature to prevent it from breaking or loosing its selective permeability.
   
What is the difference between (passive) carrier and channel proteins?
What is the difference between carrier mediated protein channels and channel mediated protein channels in the phospholipid bilayer of the plasma membrane?? (i do know that they both do not require energy...but thats it)

And I am not referring to the active transport carrier protein where energy is required to carry substances through the plasma membrane.
Carrier mediated transport involves a carrier protein. The carrier protein binds to the substance and undergoes a conformational change as it is bound to the substance. This molecule then possesses a specific shape that enables it to pass through a specific porous protein channel. Some substances do not require carrier proteins; channel mediated transport involves the substance travelling across the cell membrane via specific porous protein channels, into or out of the cell. And then as you already know, these are means of facilitated diffusion, and so are passive and require not ATP energy input in order to take place.

Hope this helped!
Are there transport membrane proteins in organelle membranes as well?
Hi,

Can transport membrane proteins (carrier and channel proteins) be embedded within the membranes of organelles as well? Not just in the plasma membrane?

Thanks  :)
They absolutely can. Mitochondria and chloroplasts both have them. Don't think any others do though I'm happy to be corrected.
Concise description of the fluid-mosaic model
Can someone give me a concise description of the fluid mosaic model? Cheers.
•   Not rigid – “fluid”
•   Irregular protein pattern – “mosaic”
Membranes are not solid structures. The various elements in the membrane aren't static, they move around in it. So by fluid mosaic, it means that the membrane itself behaves somewhat like a fluid, and in particular, embedded proteins and structures are able to move around that fluid. Membranes themselves can maintain a shape (though can also change it), just the elements in it don't stay in their places, they're free to move around.
Definition of cytoplasm
Is the following definition of a cytoplasm accurate?

'a jelly-like substance that contains the contents of a cell (except the nucleus) such as the ions, enzymes, organelles and is more than 90% water'

Why doesn't the cytoplasm enclose the nucleus?

Thanks :)

Also, I know that the cytosol is the fluid component of the cytoplasm but is it correct to say that the cytoplasm also contains cytosol since it encloses the organelles? What is the significance of the cytosol's fluidity?
Cytoplasm: the fluid within a cell which includes all cell organelles apart from the nucleus. I see it as a collective term (composed of cell organelles + cytosol minus nucleus)
Apparently, the nucleus isn't part of the cytoplasm as it contains its own fluid called nucleoplasm.

Yes, cytosol is a constituent of cytoplasm. Its fluidity is significant in that it suspends the organelles that are part of the cytoplasm. Edit: should also mention that because it is mostly made of water, many cellular reactions occur within it.
Relating to the significance of the cytosol's fluidity; I believe its fluidity is vital for overall cell functions. Can you image if it was not fluid?
From what I've read, the aspect of fluidity in the cytoplasm(which consists of cytosol) creates cytoplasmic reorganisation during cell reproduction and in some protists it provides the mechanism for cell locomotion (movement); it aids in the delivery of nutrients, cell products, and genetic information to all parts of a cell, allowing cell components to flow to all parts of the cell. So basically it's important for all intracellular functions. Hope that helps.

Edit: Think of it in terms of osmosis as well (I suppose).
Do all organelles have membranes?
I was told that organelles do not necessarily require membranes. (e.g. ribosomes are not membrane-bound) Is this true?
This is true. Some organelles (i.e. ALL those found in prokaryotic cells and SOME found in eukaryotic cells) are not membrane bound. The best example of this is the ribosome.
Osmosis: Should I refer to water or solute concentration?
Referring to osmosis, what's correct to say: a higher water concentration or higher solute con. when taking about hypo/hypertonic solutions? Or is both correct?
There were several different replies for this one, some of them were wrong so I’ll just include my definition.
“The passive net movement of free water molecules, across a semi-permeable membrane, from a region of low solute concentration to higher solute concentration.”
Passive – Does not require energy
Net movement – Some actually moves backwards, but the majority goes the same way
Free water molecules – The water molecules cannot be bonded to another molecule or they will not be able to pass through the membrane.
When mentioning low/high you need to make it clear it is solute concentration that you are talking about.
Why are membranes permeable to lipid-soluble molecules but not water-soluble molecules?
can someone please give me a more detailed explanation as to why membranes are permeable to lipid-soluble molecules, but impermeable to water-soluble molecules?
Membranes are composed of phospholipids which contain a glycerol attached to a phosphate head and two fatty acid tails. These fatty acid tails are hydrophobic non polar molecules that repel water as water is polar. Lipophilic substances can easily diffuse through the membrane however ions and polar substances require protein channels that are embedded in the membrane.
The plasma membrane is made up primarily of a phospholipid bi-layer. The fatty acid tails are hydrophobic. Because of the like-nature of the bi-layer and the lipid-soluble molecules, the molecules are able to rapidly dissolve across the plasma membrane without the need of protein trans-membrane receptors. Because of the hydrophilic nature of water-soluble molecules, they are repelled by the membrane, and so cannot dissolve readily across the cell membrane, and need receptor proteins and secondary-messenger molecules to relay the message during signal transduction.
Why aren’t lipid molecules repelled by hydrophilic phosphate heads?
Just a quick [burning] question- Why aren't lipid molecules repelled by the hydrophilic phosphate head? How are they able to overcome this and readily diffuse through the bi-layer?? I'm guessing this has something to do with the uneven proportion of phosphate vs. fatty-tails :\ ??
In the plasma membrane, phospholipid molecules do not actually "stay close" together, there are gaps between each molecule, therefore, substances that are SMALL and lipid-soluble should be able to move through those gaps and diffuse inside the cell.
Hope this helps!
This answer is only partly right. Lipid soluble molecules are not repelled by the hydrophilic heads because they are currently in a watery environment. The heads are not a hydrophilic layer, more like the barrier dividing hydrophilic from hydrophobic. The environment on one side is hydrophilic and on the other side is hydrophobic (the tails).
Function of cell membrane
Explain why a functioning cell membrane is essential to maintain the integrity and survival of cells showing your understanding of the structure of the cell membrane.
The cell membrane is selectively permeable allowing it to import and export substances needed by the cell as necessary. The cell is compartmentalized by the cell membrane making it possible for membrane bound organelles to have different compositions and achieve metabolic efficiency. These compartments are important in making sure energy is conserved and used most efficiently inside the cell by preventing interference between different reaction pathways and enabling radically different reaction environments to be accommodated in organelles.
The cell membrane is composed of phospholipids with a hydrophilic phosphate head and hydrophobic lipid tails. This means the phosphate heads point into the cytosol and the lipid tails point towards each other (diagram might help in visualizing this). The steroid cholestrol is wedged between the phospholipid molecules of animal cells and is a fluidity buffer for the membrane by resisting changes in membrane fluidity that can result from changing temperature. This is fundamental in how some animals have evolved to cope with extreme temperatures. For example, Arctic Fish have a high proportion of unsaturated hydrocarbon (kinked) tails in their membrane enabling their membranes to stay fluid. If they had saturated hydrocarbon tails packed together, the membrane would be highly viscous and would solidify in the low temperatures of its habitat, meaning the cell would lack its functionality too.
Factors that affect the rate of diffusion across a membrane
List and explain the factors that affect the rate of diffusion of substances across membranes.
Temperature - A greater temperature increases the kinetic energy of molecules allowing them to diffuse across the membrane faster.
Concentration gradient - A greater concentration gradient would mean solutes are naturally more inclined to travel from regions of their high concentration to regions of their low concentration
Surface Area - Membranes with more surface area allow more molecules to diffuse per unit of time.
Not to forget the nature of the substance itself, such as size and polarity as well as characteristics of the membrane as well.

Those very largely are what people want you to remember though, so you've definitely hit the right ones there.
Are carrier proteins active or passive transport?
I've also got another question - Facilitated diffusion: the diffusion of substances that occur through protein channels/carriers; does not expend energy.

In regards to protein carriers, [such as the Na+ K+ pump which is an example of facilitated diffusion?] how come this process is terms 'passive'? Doesn't it require energy in the form of ATP to alter the shape of the protein carrier? Or is it active transport?
Basically how does a carrier protein function and why is it classified under facilitated diffusion?

Thanks!!
Sodium/potassium pumps are active :)
So are carrier proteins used only in active transport? From what I know (which may be wrong), a carrier molecule to change its shape (to allow for another molecule to pass), it needs ATP to induce that change. So ...
You use carrier proteins in facilitated diffusion as well. They're a little bit different though. When something bumps into them, they kind of just suck it in, kind of like quick sand. Whereas ones that require ATP are more like a vacuum, they force stuff through even if there's no gradient.

So carrier proteins in facilitated diffusion use the gradient to get stuff through.
Carrier proteins in active transport use the gradient AND force stuff through.
So in active transport, only carrier proteins are used?
Is it true that only carrier protein can be used in active transport and not channel protein?
Yep, only carriers.
Can carrier proteins be used for facilitated diffusion too?
Can carrier proteins also be used for passive carrier mediated transport for specific molecules?
Carrier proteins play a role in facilitated diffusion, yep.
Do channel proteins change shape?
Just as carrier proteins change shape to accomadate the transport of substances in and out of the cell, can channel proteins also change shape? If so, can you specify in what instances?

Cheers!
In some respects. But not really. They're kind of like a real channel, fixed shape, but some have gates.
I'd think of channel proteins more as pipes really (yes the hard plastic ones under your sink). In-fact, the property that they rarely change shape is actually very important in their function in a way. You want channels only letting in what they are "designed" to let in and not everything.
Does endocytosis reduce the size of the plasma membrane?
Would endocytosis reduce the size of the plasma membrane of a cell?

Thanks!
Not by any measurable amount - vesicles from the plasma membrane are very small relative to the size of the cell
Do animal cells lyse in a hypotonic solution?
Note: ‘Lyse’ means burst
Is it correct to say that animal cells, which lack cell walls, undergo lysis when placed in an aqueous solution due to the osmotic pressure that accumulates within the cell to enable the two mediums (cytoplasm and aqueous solution) to reach equilibrium?

Thanks!
Animal cells generally undergo lysis (that is, they burst) when placed in a hypotonic solution as there is a net movement of water molecules from the region of higher water concentration - outside the cell - to the region of lower water concentration - inside the cell. This causes the cell to swell and eventually, if no regulatory mechanisms are in play, causes it to burst. I think it's important to note that osmosis will occur regardless of whether the cell is about to burst or not; so long as equilibrium has not been reached, water will continue to move into the cell. So you could probably deduce that the cell will burst before equilibrium is reached.

Edit: forgot to mention, animal cells lack both a cell wall and a large vacuole
How do substances like detergent disrupt the bilayer
How do substances like detergent disrupt the bilayer?
Please quote me if I'm wrong but the phospholipid bilayer is primarily composed of phospholipids however it has large amounts of protein embedded in it. If you've washed dishes before, you may have noticed that once you add the detergent, the oils suddenly begin to evacuate as far as possible. Similarly, the polarity of detergents puts huge amounts of pressure onto the bilayer causing it to disintegrate - I'm guessing this happens because the phospholipids try to get away from the detergent and in the process, separate from one another. (especially since the bilayer has LOTS of protein channels/pumps which makes the job easier) it's also important to note that the phospholipids aren't actually stuck to together and are instead flexible.
That's pretttttty much it, but not quite.

Detergent disrupts the phospholipid bilayer because it's made of lipids. So it's kind of like mixing coke with water, you'd expect them to just mix around. So it actually has the effect of diluting the bilayer. Because it doesn't have the same structural properties as bilayers, this means that wherever the detergent has mixed in (essentially) the bilayer won't be a layer anymore, instead, just free, happy phospholipids.
It moves around and breaks a bit, so they just slide through like it's water. Non-polar substances don't go through the gaps though, it's incorrect to say this :)
Just to make a few things clear for everyone (and if anybody does see some problems jump on them please, because it's been a little while).

As alchemy has mentioned, simple diffusion will involve small molecules or lipid soluble molecules. It's really important that you all understand this, but also understand why this is occurring. The plasma membrane is made of a phospholipid. Yes, this is an amphipathic molecule, but it probably is important to note that the major component is that lipid. The polar region is certainly much smaller. So, lipids can pass through by simple diffusion as well because it only needs to get past a pretty week polar barrier to make it into that nice, lipid environment.

Small molecules can get through because they're just that, they're small. The phospholipid bilayer can't pack in perfectly, and by virtue of the fact that the cell is at 37°C and not -273°C, the phospholipids will constantly move and jiggle around. For small molecules, they can just weave through, even if they are slightly charged. The effect of polarity isn't enough to knock them away either.

So the key points there:

-the effect of the phosphate heads' polarity will not be sufficient to deflect a lipid molecule; a phospholipid is a mainly non-polar molecule. The lipid will just barge through that tiny deflection.
-small molecules can get through for two reasons: there are tiny gaps because the packaging of phospholipids next to each other isn't perfect, and because the effect of polarity, likewise, isn't strong enough to knock them back.

Compare this last point with charged molecules. Whilst small, they bare a full charge, which would respond too much to the charge difference between itself and the phospholipid. The charge difference between an ion and a polar molecule is greater than the charge difference between two polar molecules. In this case, the difference will be great enough to keep the ions out.


The membrane is one of the most incredible things in Biology. Its design is absolutely perfect and its chemistry astounding. These systems that you're learning about, various types of transport across the membrane, reflect the complexity of its chemistry. That's why there's so much to learn, because you really are learning about an incredible structure.
Where does water move through the phospholipid bilayer?
Through which part, in particular, does water travel through the phospholipid bilayer? Simply in between the phospholipds?
Thanks
Yes :) a cell membrane is porous allowing certain small polar molecules such as water to diffuse through. This is also known as simple diffusion.
I don't know if this is part of the course, but the majority of water movement into and out of the cell is facilitated by specific membrane channels called aquaporins.

Some water does diffuse through the membrane, but it is incorrect with the current understanding of cell membrane structure to attribute water movement solely to simple diffusion.
What is the role of the cell membrane?
What is the role of the cell membrane?
The plasma membrane plays an integral role in the regulation of inputs and outputs in the cell, is involved in intercellular recognition and communication, encloses the contents within a cell and also protects a cell from its immediate environment.
If a liquid is brought out of a cell by exocytosis, is it called pinocytosis?
Can liquid brought out of a cell by exocytosis also be referred to as pinocytosis or is this term only restricted to endocytosis?

Thanks!
I think it's restricted to endocytosis.
Is active transport net movement?
Would active transport be considered as the net movement of particles or not?
Yes, but remember that it occurs against the concentration gradient thus requiring the expenditure of energy in the form of ATP for it to occur.
Absolutely. You're always talking about net movement. There is no naturally occurring (or for that matter unnaturally occurring) instance when particles aren't moving at all.
What is the definition of osmosis?
What is the definition of osmosis? Do I need to include info about the semi permeable membrane?
Thanks in advance :D
There are many different ones, use one that includes all the necessary points but that you remember. The definition I use is:
‘The passive net movement of free water molecules across a semi-permeable membrane, from a region of low solute concentration to high solute concentration.’
Is it easier for small non-polar molecules to cross the plasma membrane than it is for small polar molecules?
Is it generally easier for small non-polar substances to pass through the cell membrane by simple diffusion or is it easier for small polar substances to?

I always thought polar substances had a bit more trouble, as the interior of the phospholipid bilayer is non-polar?
Well, small non polar substances would diffuser across easier, although some small polar substances are tiny enough to slip through the tiny pores of the plasma membrane (e.g. water).
Non-polar substances can easily diffuse through the membrane and small polar molecules can as well but larger polar (hydrophilic) and charged molecules require protein channels.

The interior of the phospholipid is non-polar however the phosphate heads are not but since the membrane is porous, water molecules and certain other substances can diffuse through.

Note that the factors which affect diffusion are size, charge and polarity.
Yes, non-polar substances are able to readily diffuse through the cell membrane because it has a greater affinity for the hydrophobic region. Whilst, polar molecules such as water are able to diffuse through small spaces between the phospholipids (because of their small size), it is relatively  harder for them to break that initial barrier/repulsion to enter. But they are able to, nonetheless.
Are there non-polar molecules that are too large to diffuse across the plasma membrane?
If large molecules have trouble diffusing across the plasma membrane, does that mean even if they are large hydrophobic molecules, they will need to partake in facilitated diffusion in order to cross the plasma membrane?
Presumably there'd be a point where they got too big, but they often don't. Hydrophobic molecules can move through the membrane as though it were a sheet of water.
What can/cannot readily pass through the plasma membrane?
What can/cannot readily pass through the cell membrane?
Preferably 2-3 sentences.
Thanks ;)
I will have a try at this. Non-polar/ uncharged/ small molecules can pass through membrane. Whilst large, charged, polar molecules can not pass through the plasma membrane unless aided by a membrane protein. Don't trust me In just guessing, someone please correct me
Facilitated diffusion definition
If anyone can clarify the following that would be greatly appreciated :)

Would you say that facilitated diffusion is the passive, net movement of particles from a region of high concentration to a region of low concentration, via transmembrane proteins?
Or do you have to specify carrier/channel proteins?
Thanks
I think it would be better to say ' through specific channel/carrier transmembrane proteins'. Also, I think you should specify what type of particles pass through the proteins; so large, polar and charged molecules perhaps.
What substances are found in the plasma membrane?
What substances are found in the cell membrane?
Protein carriers, protein channels and cholesterol.
The membrane itself is primarily composed of phospholipids and carbohydrate chains (glycolipids and glycoproteins) are attached to some protein channels and phospholipids on the surface of the membrane.
What is the effect of turgor pressure in plant cells?
what is the use of turgor pressure in plant cells?
To give the plant rigidity.
It also stops the cells bursting (lysing) when placed in a hypotonic solution.
Structure of the membrane of organelles
Can someone describe the structure of the membrane of organelles?

Do they also have protein channels, etc.?

Also, is ribosome referred to a  non-membrane bound organelle because it does not have a phospholipid bilayer? If so, what is the membrane of ribosome like?

Thanks!
The structure of organelle membranes is pretty different to that of the cell itself, but in a very broad stroke, they are essentially the same kind of thing. Phospholipid and whatnot, most will have protein channels though it does depend on the organelle. FOr example, you should already have some insights into the membrane of most of the organelles you've already encountered. A little bit of a recap:

Nucleus: bilayer that folds in on itself to make pores.
Mitochondria: internal and external membranes, lots of membrane proteins particularly in the internal membrane (think ETC). Naturally, there are channels/carriers on the external membrane to let proteins in and out
Chloroplast: similar story to mitochondria, two membranes (gram -), thylakoids on the inside
ER: pretty similar to cell, though studied with ribosomal complexes
Golgi: practically identical to the cellular membrane. Pretty much all golgi membrane eventually becomes cell membrane anyway, so they have to be very similar. Although, the membrane in the Golgi actually undergoes changes, becoming more and more structurally similar to the cell as it gets closer to budding off.

Ribosomes don't have a membrane at all. They're just a big hunk of protein and rRNA
Does the steepness of a concentration gradient affect the speed of diffusion?
Can it be said that a small-scale concentration gradient between two solutions means that osmosis would occur at a slower rate?
Absolutely! This is a really important factor in diffusion and osmosis. The larger the conc. gradient, the faster the rate of diffusion/osmosis.
Do endocytosis and exocytosis require energy?
Does endocytosis and exocytosis require energy?
Yes - they are both active processes.
What is meant by [b
net[/b] movement?]
In diffusion and osmosis what is meant by net movement of a substance/water molecules?
In reality, the particles move in both directions but due to the concentration gradient, the overall movement is down the concentration gradient. Even in equilibrium when the concentrations are the same, the particles are still moving between the solutes but there is no overall movement (change in concentration).
What is a protein channel?
What is a good definition/explanation of a protein channel?
A protein channel is a protein embedded in the plasma membrane which facilitates the movement of particles across the membrane by facilitated diffusion or active transport.
How do you define hypertonic/isotonic/hypotonic?
Just wondering how would you define the words hypertonic, hypertonic and isotonic?? I know what they mean just not sure how to define them. Thanks
Hypertonic describes a solution in which the solutes are more highly concentrated than the solution with which you compare it.
Isotonic describes two solutions with equal concentration of solutes.
Hypotonic describes a solution in which the solutes are less concentrated than the solution with which you compare it.
Is it the cholesterol in plasma membrane that allow for the membrane to reseal itself?
Is it the cholesterol in plasma membranes that allow for the membrane to reseal itself if it is punctured?
Cholesterol assists membranes in maintaining their structure, so yes it would help. The hydrophobic attractions between the tails of phospholipids, however, will provide membranes with the means for repairing themselves. Just think about the polarity of a phospholipid and the hydrophobic and hydrophilic ends.
Does cholesterol increase or decrease fluidity of the plasma membrane?
Does cholesterol increase or decrease the fluidity of membranes?

In some sources I have come across, it says cholesterol increases the fluidity of membranes but others say they add a level of rigidity to membranes?

Does anyone know which is actually correct?
o.O
Cholesterol actually increases or decreases fluidity depending on the temperature!

At low temperatures, the cholesterol will make the phosphilipid bilayer more fluid in order to prevent solidification, whereas at high/moderate temperatures, the cholesterol will reduce the membrane's fluidity.
It's actually both, funnily enough. Cholesterol serves to give the membranes both fluidity and rigidity in different conditions. It is a 'bidirectional regulator' of membrane fluidity.

When environmental temperature is high, cholesterol gives the membrane rigidity by raising the membrane's melting temperature, while at low temps it acts to prevent the membrane from stiffening and becoming too rigid.

edit: beaten by howlingwisdom haha
Are there channel/carrier proteins in the membrane of organelles?
Are carrier proteins and channel proteins only situated on the surface of plasma membranes or are they on the membranes of other organelles within the cell as well?
Yeah, organelles are bound by plasma membranes that include various transport proteins (eg. channel proteins)
What is the difference between cytosol and cytoplasm?
Cytosol and cytoplasm.
What are the differences?

Getting confused  :/

Thank you
Just think of it this way. Cytosol is a part of the Cytoplasm. More specifically, the cytosol is the fluid-like inside of the cell. The Cytoplasm is more of a collective term for the Cytosol including the organelles suspended within the Cytosol.
What is meant by internal or external environment?
What is the meaning and difference between internal environment and the external environment?
Well it depends. The internal environment of an organism is the extracellular/interstitial/plasma fluid in which its cells are surrounded by. The external environment is everything else.

The internal environment of a cell is the cytosol within, whereas the external environment is the extracellular fluid which surrounds the cell.

Confusing? It is.
How do molecules cross the plasma membrane?
Beware, silly question:
How does anything just diffuse through the cell membrane, do substances just go though gaps in the cell membrane?
Even then wouldn't it face forces of attraction from the hydrophobic tails? E.g. in the case of lipid movement through the cell membrane. Wouldn't dispersion forces act between the lipid and hydrophobic tails therefore causing it to 'get stuck'  for some periods of time
Pretty much. As the plasma membrane is fluid-like, pores appear between the phospholipids and hence certain molecules are able to diffuse across. Remember that dispersion forces are often disregarded due to their relative weakness, and as such, do not really inhibit the diffusion of substances (I think, at least for VCE Bio :p).
Not a silly question at all :)
So a lot of molecules like oxygen and water will freely diffuse across the plasma membrane, since they're relatively small.
For larger molecules like sugars and amino acids they diffuse via a process of facilitated diffusion, where they bind to membrane-spanning transport proteins and diffuse across through protein conformational changes; this doesn't require energy.
For ions moved against their concentration gradient, active transport is used - i.e. energy demanding. A classic example is of course the K+/Na+ ATPase pump.

I am not 100% here, but I don't know if lipid diffusion is in Biology 3/4; lipid diffusion is a bit more complex than the former.
Why is it important to have a large surface area? What does it indicate about the cell?
Hi!!
Can someone please help me with the explaining the crucial role of membrane systems and organelles for increasing the total membrane surface area within the cell? I'm not too sure on this one :(
Essentially, it increases the efficiency of the cell. A larger surface area provides a larger area for substances to move in/out of the cell or organelle, or it increases the rate of specific reactions (e.g. Oxidative Phosphorylation in aerobic cellular respiration) that occur in membranes.
To add to what grannysmith said, it follows that things that are super super super folded, are doing a lot of reacting or a lot of transporting—or at the very least have the capacity to do so. So, for example, you know that mitochondria are really trying to get a lot of bang for their buck because the membrane is folded so much.
Why can water molecules diffuse across the plasma membrane?
Also, how do water molecules freely diffuse through the membrane if the region between the membrane is non-polar (lipophillic) ?
Water molecules are so small that they can easily move through the (transient) pores in the plasma membrane.
Oh, alright so they don't actually go 'through' the phospholipid bilayer, right?

They do, but I get where you're coming from :p

Remember that the plasma membrane is a fluid, as the phospholipids are constantly moving around. This allows temporary 'holes' to appear in the membrane; albeit small, they're large enough for water molecules to go through.
Definition of diffusion, osmosis, active transport
Hi guys!

Ridiculously easy question... what would be a good/concise definition for diffusion, osmosis and active transport?
Does anyone have a definition given by VCAA from past exams?


Thanks :)
Diffusion: The passive net movement (down a concentration gradient) of a solute from a region of high solute concentration to a region of low solute concentration.

Osmosis: Passive net transport (again, down a concentration gradient) of a solvent (almost always water for the purposes of VCE biology) from a region of low solute concentration to a region of high solute concentration. This process usually takes place across a semi-permeable membrane.

Active transport: Active (therefore requiring energy as ATP) net transport of a solute from a region of low solute concentration to a region of high solute concentration (therefore up a concentration gradient).




I've colour-coded some important bits of those definitions, because students often get confused between solvents/solutes and the like :)

"Net" is highlighted as such as it is important to remember that solutions are NOT static; there is constant flow between regions. Hence, we can identify changes only as NET movements of solutes relative to solvent concentrations in regions of a solution.

Hope this helps!
What is meant by ‘net movement’?
osmosis is the 'net movement'

What exactly is meant by net movement?
The overall movement of water molecules, ex. more molecules are moving in to the cell than out, therefore net movement is into the cell.
If it's the overall, then does that mean 'some' water molecules are going in the opposite osmotic direction?
yeah you can’t ever have a 100% of the water going in one direction
How does the structure of the plasma membrane affect the movement of different substances across it?
Hey everyone!
I'm a bit stuck on this question "Explain how the structure of the plasma membrane affects the movement of different substances through it"
Basically I'm not to sure whether to talk about the (or even mention) the fluid mosaic model, or whether to talk about the selective permeability and substances etc. Thanks :)
Well,

The fluid mosaic model describes a phospholipid bilayer with embedded proteins. Such a structure contains phospholipids with hydrophilic heads and hydrophobic tails, allowing lipid soluble substances to pass through the membrane with ease. However, larger molecules need to enter the cell via other methods, and this is where the role of proteins is vital, with features such as protein channels and carrier proteins becoming essential in ensuring passage for certain substances across the membrane. As you can see, this selective permeability can be owed to the fluid mosaic model of the membrane, tying your two points together.

I hope that's what you were asking  ;D
Is facilitated diffusion active or passive?
Can facilitated diffusion be both active and passive?
I think it can as both FD and AT use carrier proteins idk i might be wrong.

Thanks in advance :)
No, facilitated diffusion uses both carrier proteins AND protein channels, however, they require no energy at all as they go from a high concentration to a low one. Active transport ONLY uses carrier proteins, and requires energy because it goes from a low concentration to a high one.

I think were you're confused is 'oh how come two processes can use carrier proteins'?
Well, active transport and facilitated diffusion use them. There is only one different, if a substance is going down its concentration gradient, then it's facilitated. If the substance is going against it's concentration gradient, then it's active.

Hope it helped :)
What do we need to know about a eukaryotic cells skeleton?
What do we need to know about a eukaryotic cell's cytoskeleton??

 Is knowing that the cytoskeleton is a network of protein fibres which provide structural support, anchorage, shape, motility and a capacity to move and arrange organelles within the cell sufficient? (i got this definition off a website, not sure if it's right though)

Yep, that's more than enough.

Simple/facilitated diffusion, osmosis, active transport
Hello everyone!  ;D

I would just like to ask if anybody could explain the modes of transport of soluble substances across the plasma membrane. And explain each of the following: Simple diffusion, facilitated diffusion, osmosis and active transport.

Thanks.
Well in Biology, when the word 'soluble' is used, it typically describes a molecule (group of atoms) that are able to dissolve in water. So when we talk about soluble substances transporting across plasma membranes, then were talking about molecules, that are able to diffuse in water, that can simply diffuse through the membranes.

Simple diffusion:
This is the process where either small, non-polar substances can simply diffuse through the cell membrane of cells, because the chemical nature of the membrane is lipophilic, and so the non-polar (lipophilic) substances can diffuse through, as they are attracted to the fatty acid chains. Also, some polar, relatively small molecules such as water and carbon dioxide can still diffuse simply through the plasma membrane, despite being polar, and despite being repelled from the fatty acid chains of phospholipids, because they're so small and can just go through the small pores of the membranes. Remember, simple diffusion is diffusion, the movement of particles from a relatively HIGH concentration to a region of LOW concentration, ALONG the concentration gradient. Diffusion is passive; it does not require energy to proceed (ATP).

Facilitated diffusion:
Facilitated diffusion is the process where particles/molecules are transported from a region of relatively HIGH concentration to a region of LOW concentration, ALONG the gradient, through a plasma membrane with the FACILITATION (aid) of a protein channel/carrier. So, this means that when a molecule is too large, and possibly also polar, and hence cannot freely/simply diffuse the plasma membrane, then it must use some other scheme of transport, right? In this case, these relatively large, polar molecules, such as glucose, will need to be transported into/out of cells through proteins molecules that are pre-embedded into the membrane. This process is also passive; it does not require energy (ATP).

Osmosis:
Osmosis is literally the diffusion of water molecules, through a plasma membrane in/out of cells. Osmosis occurs when water molecules exist at a higher concentration, and diffuse inside a cell, where their concentration is relatively low. Diffusion occurs until equilibrium is achieved, that is, when the amount of water is equal both inside and outside the cells. Osmosis is passive; it does not require energy (ATP).

Active transport:
This is the transport of molecules from a region of relatively LOW concentration to a region of HIGH concentration, AGAINST the concentration gradient, through a plasma membrane. Active transport occurs when molecules from low to high, and this process occurs actively, that is, it require energy to occur (ATP).

I hope this helped xD
The way substances are transported across a membrane is determined by 2 things - polarity and size.
If something is small it will move much more easily through the membrane than  if it is large.
If something is polar it will not move through as easily as something that is non polar.
Diffusion or the movement of a substance is affected by - temperature  and steepness of the concentration gradient.
Concentration gradient refers to the difference between the concentrations on either side of the membrane. If one side has an extremely higher concentration than the other than the concentration gradient is steep and diffusion will occur. Diffusion is passive (means no energy) the movement of particles from an area of high concentration to an area of low concentration so a some sort of balance can be achieved. This just entails the particles simply passing through the membrane and no energy is required.
However, the diffusion of water (if we can call it that) is referred to as osmosis. Osmosis is the movement of water particles from an area of high free water particles to an area of low free water particles. So if you have a solution separated by a semi permeable memberane (one that only allows the movement of some particles and not other) water will move from the side that has more free water particles (that is , water particles not bonded to the solute) to the area where there is less (that is , the area where most water particles are bonded to solute particles) .
But remember the conditions (polarity and size) that I said earlier. If a particle is large or polar , due to the nature of the phospholipid bilayer it cannot simply diffuse across the membrane so it undergoes a process known as facilitated diffusion. This entails the use of a membrane protein that aids in transporting the substance across the membrane. This happens still following the concentration gradient , so particles move using the protein from an area of high concentration to an area of low concentration.
Now how about if something doesn't want to follow the concentration gradient and wants to instead go from an area of low concentration to an area of high concentration? Then active transport occurs. This requires energy.
Hope this helps  :)
Edit : beaten by cosine
What determines whether a molecule goes through a channel or carrier protein? Can they go through both?
Hey guys,
I'm having a bit of trouble understanding the two types of facilitated diffusion - carrier and channel mediated.

I have a couple of questions:
1) Is there a difference between molecules going through channel and carrier proteins? In other words, what determines a molecule going through the channel or carrier protein?
2) Can molecules go through both a channel and a carrier protein? In other words, can a molecule use a channel or a carrier protein, or are there specific molecules that can only go through each protein channel?


I may have been a bit confusing in my explanation, so if you need clarification I'll be happy to try explain again!

Thanks in advance guys
1. The key difference between channel and carrier proteins is their tertiary structures. Channel proteins, quite literally, form a channel through the plasma membrane. If the right molecule can fit into the channel, it will simply fall through. Carrier proteins, on the other hand, must be deformed to pass through a molecule. Such that, the shape of the carrier protein changes as it conveys its cargo across the membrane.
Whether or not a molecule goes through a carrier or a channel protein depends really on what's available. There are some molecules (e.g. ions) that tend to go through channels and so on, but really there isn't a solid way of differentiating between the two.

2. Theoretically, yes. Not sure I can think of an example of something that actually does though.
Why is there a non-polar region in the phospholipid bilayer?
2.  In the phospholipid bilayer, why is the head polar, while the tails are non-polar? Because doesn't that mean that even if water can get through the head, it won't be able to get through the middle of layer (non-polar tails)?
2. The reason for their polarity just comes down to the fact that the heads are charged and the tails are long alkane chains. Water can get through because it can, effectively, sneak past the tails.
What is osmotic pressure?
Hey could somebody give an explanation of what is osmotic pressure and give a definition of it as well???
Osmotic pressure is the pressure that is referred to when water diffuses into the high solute concentrated region. It's like a measure of the concentration of solute, the higher it is, the osmotic pressure would also be larger because the water wants to equilibrate the concentrated solute even more, where as if there is such low concentration of the solute, then there would be less osmotic pressure because the water isn't pressured that heavily to equilibrate the solute. Hope this helps xD
Why do people spray water on fruit and veg in supermarkets?
Why do people spray water to fresh fruits and vegetables in grocery stores? Is it to maintain turgor pressure. Can someone explain??
Water is sprayed so that it can simply diffuse through the fruit cells and the cells will now have an excess of turgor pressure, meaning they will swell up and hence will look more appealing to the eyes of customers.
Is there a difference between an organelles membrane and a cell membrane?
- Generally what are the differences between the cell's membranes and its organelles membrane's in terms of structure and composition?
Thanks.
- There is no difference, generally (for the purpose of VCE).

Hopefully this helped you out a bit. Keep working hard!
How does temperature affect osmosis and simple diffusion?
Can someone explain the following

1) how does temperature effect osmosis? lets say a cell is placed into a lower solute concentration solution ( hypo tonic ), and lets say another cell is also place in a hypotonic solution but at 50 C degrees, I understand that osmosis may occur quicker in the later but I don't understand the logic behind it since a reaction isn't occuring so it is not a case of reaction rates :P
2) same as above but for simple diffusion
1). Temperature affects the rate of osmosis because higher temperatures will increase the kinetic, molecular energy/movement of molecules, so the water molecules have a more rapid rate of diffusing through the membrane. Likewise with low temperatures, the molecular kinetic energy is reduced, so the water molecules move relatively slower, hence rate of osmosis is reduced too.

2). Same as above xD
« Last Edit: November 27, 2018, 02:15:12 pm by PhoenixxFire »
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Re: Biology Q&A archive/Bio FAQ
« Reply #2 on: April 09, 2018, 09:29:17 pm »
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U3 AOS 1 Plasma membranes part 2
Relevant study design dot points
• the fluid mosaic model of the structure of the plasma membrane and the movement of hydrophilic and hydrophobic substances across it based on their size and polarity

• the role of different organelles including ribosomes, endoplasmic reticulum, Golgi apparatus and associated vesicles in the export of a protein product from the cell through exocytosis

• cellular engulfment of material by endocytosis.

Can bulk transport occur against the concentration gradient?
- Can endo/exocytosis happen down as well as against the concentration gradient?
Yes, endo/exocytosis is not limited by the concenteration gradient. It is used whenever bulk transport is needed.
- Can endo/exocytosis happen down as well as against the concentration gradient?
Endocytosis is from high to low. Just think about when pathogens are endocytosed by phagocytes, the pathogens are going from a high to low concentration. Also think about when Amoeba organisms absorbed water in bulk in their watery environment, obviously from high to low concentrations. Also, exocytosis typically occurs from high to low concentrations, such as when production of antibodies from plasma B cells is occurring, the antibodies are being produced at a rapid rate inside the cell and accumulating, and the exocytose outside the cell into the tissue. However, this knowledge is not required for VCE, just know that endo/exo are active transport and require energy (ATP)
Can large non-polar molecules cross the plasma membrane?
- Can large hydrophobic molecules pass through the membrane?
Probably not, the gaps between the phospholipids are not big enough. It would probably use endo/exocytosis (think of a white blood cell engulfing a pathogen)
- Can large hydrophobic molecules pass through the membrane?
No, not directly through the membrane, they are too large and hence can puncture the plasma membrane. Instead, they can endocytose through the membrane. However, small hydrophobic molecules such as alcohol can indeed pass through via simple diffusion.
Why is a higher surface area to volume ratio more efficient?
can someone explain ( preferably in exam language :P )
why a higher Surface area to volume ratio is more efficient?
To use exam language, might need to know the context of the question so it can be related to the stem. I'll use plant leaves as an example:
-Allows more area of absorption of sunlight by chlorophyll
-Allows photosynthesis to occur at a faster rate
-Allows more energy to be produced due to glucose produced
But also things such as diffusion (simple and facilitated), and with enzymes & substrates.
Do carrier proteins conducting facilitated diffusion need ATP?
Do carrier proteins used in facilitated diffusion ever use energy? I thought they were always passive?
Carrier proteins in facilitated diffusion are passive, carrier proteins in active transport require energy
Are endocytosis/exocytosis active transport?
6. Can endo/exocytosis be considered forms of active transport?
6. Yep! They are definitely active transport - Generally anything that doesn't have diffusion in its name is active.
What is compartmentalisation? Why is it important?
Hi, can someone explain compartmentalization i dont get it?

Hey,
Basically it allows different environments. It is when an area is separated from its environment by a membrane.

For example one organelle might need more of a substance than another organelle. Compartmentalisation means that the organelle can pump that substance inside and keep it there in higher concentration.

This also works between cells, for example a heart cell might need more glucose than blood cell. If there wasn’t compartmentalisation, they could not have different concentrations. This also applies for allowing slightly different conditions, eg. pH

Imagine your street is an organism. Each house is a cell (compartment). It’s a really hot day, so you all have your air conditioners on, but you’re all fussy people and like having your aircons set to different temperatures. If the house walls (cell membrane) were not there, you could not have different temperatures, and the cool air would escape into the street.

Does active transport use carrier proteins or channel proteins?
Does active transport use only carrier protein or only channel protein or both? I think its just carrier but im not sure.

This question is asked every year and it is sometimes quite unclear generally active transport occurs via a carrier protein but there are exceptions. For the purposes of vce it would be safe to assume that only carrier proteins are used for active transport.

Why does the ‘steepness’ of a concentration gradient affect the rate of diffusion?
Why is it that the greater the difference in concentration gradient, the faster the rate of diffusion?
lets say I have 80 molecules on the left and 0 on the right with a semi-permeable membrane in between. The left is going to be super crowded compared to the right, and the molecules will keep bouncing away from each other. On the right, there is going to be heaps of room, and less for the molecules to bounce off from. This means that the molecules will go to the right much faster than they go to the left.

If I had 50 molecules on the left and 30 on the right, we'd still have them going to the right faster than they go to the left, but not by as much.

You can also think about it as "steepness" the higher the gradient, the more steep, the faster (net) change occurs
Hope this helps.
What’s the pathway for intracellular and extracellular protein transport?
Hi
I just wanted to clarify:
1. Is the Golgi apparatus involved in transport of proteins both for use by the cell and export from the cell?
2. Which pathway would cell membrane proteins be transported via?

Thank you very much
1. Just export
2. I believe export (they'd be in the membrane of the vesicle which would then fuse with the cell membrane). But you don't need to know for VCE.
Does active transport solely use carrier proteins or can it also use channel proteins?
Hi everyone,
Wondering whether active transport solely uses carrier proteins or also can use channel proteins (which open and close)?
Active transport just uses carrier proteins.

Facilitated diffusion can happen via either channel or carrier proteins though (but you should just talk about channel proteins for VCE).
Is it true that prokaryotes lack membrane-bound organelles?
Would it be correct to state that prokaryotes completely lack any membrane-bound organelles? I have a biology 3/4 teacher who is saying that VCAA states that ribosomes have a membrane and thus the statement is wrong, but my previous teacher and every single result on google is saying otherwise. Is there any official information I can find that confirms the correct answer?

Thanks in advance.
Ribosomes are not membrane bound and prokaryotes do lack membrane bound organelles.
How does pH affect the structure of the membrane?
Would someone be able to explain to me how different pH values (2, 6 and 10) affect the structure of the cell membrane? Do both very acidic and very alkaline solutions denature the membrane structure or is it just very acidic solutions?

thanks!
Well firstly, we have to understand that pH measures the concentration of \(H^+\) ions present. And therefore, because the secondary structure of proteins is completely formed via the hydrogen bonding interactions which occur in the backbone, if we increase the number of hydrogen ions/ decrease them, this can subsequently affect the secondary structure. Also, hydrogen bonds can form between R groups in the tertiary structure, so varying pH can affect them as well.

I'm pretty sure that both very acidic and alkaline conditions can denature a protein, but just remember, it must deviate significantly from the optimum pH, otherwise we don't consider it to be denatured.
While from some quick reading it seems that pH can have effects on the integrity of the phospholipid bilayer itself, For VCE biology, you would not need to know any of this. What you need to know is rather how proteins (like those interspersed within the bilayer) can be altered (as darkz has described above).
This standard relationship between enzyme activity (approximately indicating the integrity of the protein) might help you with your query
(Image removed from quote.)
Where are the contents of the vesicle released in endocytosis?
In endocytosis, are contents released into the cytosol or in the golgi apparatus?
Cytoplasm

U3 AOS1 Nucleic acids and proteins
Relevant study design dot points
• nucleic acids as information molecules that encode instructions for the synthesis of proteins in cells

• protein functional diversity and the nature of the proteome

• the functional importance of the four hierarchal levels of protein structure

• the synthesis of a polypeptide chain from amino acid monomers by condensation polymerisation

• the structure of DNA and the three forms of RNA including similarities and differences in their subunits, and their synthesis by condensation polymerisation

• the genetic code as a degenerate triplet code and the steps in gene expression including transcription, RNA processing in eukaryotic cells and translation.

Are there Disulphide bridges in the secondary structure of proteins?
Can secondary structures contain disulphide bridges or are they only limited to tertiary structures?
Disulphide bonds are a characteristic of tertiary protein structures. :)
Which way is DNA transcribed?
what is the orientation of the leading strand in DNA replication?
I get confused whether its read top to bottom or bottom to top!
thanks
Leading strand is synthesised at its 3' end
DNA polymerases only add nucleotides at the 3' end; synthesis from 5' to 3'
So the template strand is being read 3' to 5'
I think that answer is a bit confusing.
DNA is read 3’ to 5’ and the new strand is created 5’ to 3’. Nucleotides can only be added to the 3’ end of a DNA/RNA strand, and the strands run antiparallel (in opposite directions).
The synthesis of a new strand always occurs 5' to 3' (which means that its always read 3' to 5'). This is because of the hydroxyl group on the 3' carbon, which is necessary in joining two nucleotides together.
How many nucleotides make a polypeptide?
I got this question on a practice paper, can somebody please explain how this is the answer?
Q: A polypeptide found in the cytoplasm of a cell contains 30 amino acids. How many nucleotides would be required in mRNA for this polypeptide to be translated?
A: 93
Well one amino acid is complementary to 3 nucleotides. Therefore 30x3 is 90 amino acids. Since this is a polypeptide, it means there is a stop codon, which also is coded for by an additional 3 nucleotides. 90+3+93. So all in all, there are 93 nucleotides in this polypeptide.
Which organelles are involved in producing a neurotransmitter(protein)?
Which organelles would be required to produce neurotransmitter molecule within a neuron?
Would it be enough to say ribosomes, or would I have be more specific and mention ribosomes on the rough endoplasmic reticulum?

How do neurotransmitter molecules exit the axon terminal to reach the synaptic cleft?
Golgi apparatus package neurotransmitters into secretory vesicles which exit via exocytosis. Or would it be enough to say that they exit via exocytosis?
I'd say the ribosomes on the rough endoplasmic reticulum. Any polypeptide that is synthesised by a cell, and carry out their biological function outside the cell of production, are synthesised in the ribosomes studded on the endoplasmic reticulum organelle.

When an action potential arrives at the axon terminal, this triggers an influx of Ca2+ ions. As a result, this triggers the exocytosis of neurotransmitter molecules (which are found in small, synaptic vesicles). Once they are secreted by exocytosis (an endergonic process), they diffuse across the synaptic cleft, bind to post-synaptic receptors and carry out their excitatory or inhibitory function.

Hope this helps :)
PS its good to be as succinct as possible. Assessors love punchy, succint answers that are very clear! :)
Differences between proteins produced by free ribosomes/rough ER
What type of proteins do 'free' ribosomes in the cytosol manufacture? I know ribosomes studded on the Rough E.R manufacture tertiary level proteins?
Also, does the E.R secrete its contents for the cell or for external cells? Can someone clarify this please? Thanks!
Both free ribosomes and ribosomes on the rough ER synthesis tertiary level proteins. The only difference is that proteins synthesised by the ribosomes on the Rough ER are packaged into vesicles and sent to the Golgi for further modification before being released via exocytosis.
Free ribosomes are the site of protein synthesis, for proteins that carry out their biological function within the cells they are produced. Ribosomes studded on the endoplasmic reticulum, which forms the rough endoplasmic reticulum organelle, synthesise proteins that carry out their biological function outside the cell in which they are produced.

The endoplasmic reticulum is an organelle made up of a network of membranous sacs, transporting substances within the cell and also partially modify the substances transported within the cell. It is the golgi apparatus that packages synthesised materials into vesicles that bud off the golgi body, and transport the synthesised materials out of the cell by exocytosis.
Do the smooth and rough ER interact (and what is the sequence of organelles)?
Can the smooth and rough E.R interact; does it always have to follow the sequential steps of E.R > Golgi complex > vesicle?
The smooth endoplasmic reticulum synthesises lipids and transports them within cells, whereas the rough endoplasmic reticulum synthesises proteins and transports them within cells. So no, they don't react.

Yes, the step is rough endoplasmic reticulum --> golgi complex --> vesicle!
Concise description of denaturation
Can someone please provide a concise definition of 'denaturation'? One that possibly encompasses the following points:
  • It's irreversible
  • Loss of 3-dimensional shape.
  • Results from an altercation of bonds.
  • Rendering the protein non-functional
  • Is caused by a variety of factors

Cheers!
You're pretty much already done! haha

"Denaturation is the irreversible loss of 3-dimensional protein shape due to the alteration of intra-molecular bonds. This is due to environmental factors such as heat or pH, and renders the denatured protein non-functional".

:)
Transcription and Translation in plain English
Can anyone explain transcription and translation in easy words?
Transcription is the RNA production from a DNA template. It can occur in the nucleus, mitochondria or chloroplast in Eukaryotes. Base sequences in DNA (triplet codes) are copied onto an m-RNA molecule as codons.
Translation is when the base sequence in mRNA are used to produce an amino acid sequence of a polypeptide chain, which folds to become a protein.
What is the difference between a condensation reaction and polymerisation?
What is the difference between condensation reaction and polymerisation? According to insight past paper the answer to question what is the name given to the process where monomers join to become macromolecules?? Thanks
A condensation reaction is one in which reactants combine real easing water with the product.
A polymerisation reaction is one in which monomers combine to form a polymer. ( I think this is the answer that you are looking for )
However, note that fats does not have a monomer, hence, polymerisation does not occur for this case, you have to read the question carefully.
A condensation reaction is a type of polymerization reaction. The two types of polymerization are 'addition' and 'condensation'. In addition polymerization monomers bond together without the loss of any atom or molecule. In condensation polymerization monomers bond together as well but a molecule, usually water, is lost during the process.
What elements do DNA and RNA contain?
Do both DNA and RNA contain the elements, carbon, hydrogen, oxygen, nitrogen and phosphorus?

Thanks.
Yes :) They're both nucleic acids and all nucleic acids contain carbon, hydrogen, oxygen, nitrogen and phosphorus.
Why do scientists study the proteome rather than individual proteins?
Why do scientists study the proteome of an organism, instead of single proteins?

Thanks!
Most proteins do not act in isolation, most of them interact with other proteins. So by studying the proteome, scientists are able to discover more information about them, compared to a single protein.
Why is Nitrogen an essential inorganic element for all organisms?
Why is nitrogen an essential inorganic element for all organisms? :(
Think back to the composition of biomacromolecules. Which classes of biomacromolecules require nitrogen as part of their structure?

Answer
Proteins (CHON(S)) and Nucleic Acids (CHONP(S))

Without nitrogen, these biomacromolecules couldn't exist.
Does the golgi apparatus only package and export proteins?
Hi all, can someone tell me if the golgi apparatus packages only proteins? or does it package and export other materials as well? Thanks!
Yup it packages other organic molecules into vesicles for export into the membrane or from the cell.
For VCE, you only need to know that it modifies and packages proteins into membrane bound vesicles.
Role of smooth/rough endoplasmic reticulum
Does the smooth endoplasmic reticulum synthesise lipid based hormones?
Yes. And Rough endoplasmic reticulum synthesis protein based hormones.
What is a condensation reaction?
I'm unsure of the first point in the study design:
"synthesis of biomacromolecules through the condensation reaction"
What is the condensation reaction?
Polymerisation reactions produce water as a biproduct. That's condensation. An organic reaction that produces water.
The condensation reaction refers to two molecules combining together to form one, with the release of a water molecule.

In relation to biomacromolecules, monomers (amino acids, monosaccharides, nucleotides) will undergo condensation reactions to form polymers. E.g. two amino acids will join by condensation reaction, releasing a water molecule in the process
What happens in protein synthesis?
Can someone please explain what exactly happens in protein synthesis? (Like the RNA, transcription stuff)
I'll try to cover as much as I can (in a VCE level obviously)

1. Transcription: when a gene becomes active, it will make a "mobile" copy of its genetic instructions that can transfer to the ribosome, since it cannot leave the nucleus. This genetic copy take form of RNA.
RNA polymerase unzips DNA, this enzyme (RNA polymerase) collects free RNA nucleotides that can complementary pair with the DNA template strand. A three base sequence of DNA is called "triplet", a three base sequence mRNA is called a "codon" and a three base sequence tRNA is an "anticodon", all of these 3 base sequence codes for an amino acid.

2. Translation: this is where the synthesis of protein start to take place, everything is determined by the codon of mRNA. Ribosomes will attach to mRA and start translation. Firstly, each codon on mRNA is translated by the process where tRNA carries a complementary amino acid  (i.e anticodon) to fit the codon of mRNA and make sure we obtain an exact amino acid sequence. Codon and anticodon pair using H-bond, and the polypeptide starts to grow from peptide bond. After this tRNA that carries a specific amino acid finish its mission, it will be released back and again can be used to supply the same type of amino acid over again. Finally, in order for translation to stop, a protein molecule, called release factor will occupy the codon site, create a "stop codon", also the bond between the last amino acid and the last tRNA is broken, release a free polypeptide. the ribosomal subunit ultimately break free the mRNA.
Still confused, try this video which contains more detailed and visual explanation https://www.youtube.com/watch?v=ZNl1z6Lev1E
Hope this helps!
Role of mRNA/tRNA/rRNA
Can someone pls explain mRNA, tRNA and rRNA?
Transcription in the nucleus produces messenger RNA (mRNA) which carries genetic information or in other words nucleotide bases from the DNA strand to ribosomes. It is basically a chemical blueprint in protein synthesis.

Ribosomal RNA (rRNA) is produced in the nucleolus and is important for structural support of the ribosome as it comprises much of the ribosome.

Transfer RNA (tRNA) is a also a single stranded RNA that carries an amino acid to ribosomes. It contains 3 bases known as anti-codon and carries the amino acid to the ribosome only if these anti-codon correspond with the codon or 3 bases of the mRNA.
Why does DNA replication only occur 5’ to 3’?
why does dna replication start from 5' to 3'? why cant it be the other way around?
Shape of the enzyme. It only binds the 3' end of DNA.
Roles of the enzyme RNA polymerase
What would be 2 roles (functions) of the enzyme 'RNA polymerase'??
RNA polymerase is an enzyme that binds to a specific section where an mRNA will be synthesised. Then a DNA strand unwinds, the RNA polymerase initiates mRNA and moves along one of the DNA strands in the 3' to 5' direction. Resulting in a mRNA molecule.

So basically it functions in synthesising mRNA.
Which way is DNA transcribed?
This was in relation to the above question:
Isn't it in the 5' to 3' direction?
RNA polymerase adds nucleotides in a 5' to 3' direction, during transcription. but RNA polymerase moves along the DNA template strand in a 3' to 5' direction, during the transcription process.
This is because DNA is antiparallel – If you’re building 5’ to 3’ the complementary strand (the template) must be 3’ to 5’.
Why is a ribosome needed for translation?
Why does translation occur on a ribosome, why can't the tRNA just associate with the mRNA?  :)
Because the ribosome synthesises a polypeptide from the amino acid that the tRNA carries. If the tRNA and mRNA simply associated in the cytosol, then there would be no way to synthesise a polypeptide chain.
Do START and STOP codons code for an amino acid?
In protein synthesis, do the START and STOP codons cause an amino acid to join the chain? Eg. If I had START xxx xxx xxx STOP would 5 or 3 amino acids be on the chain?
The start codon (AUG) codes for methionine, which is an amino acid that would be added to the chain. Stop codons don't code for any amino acids and merely signal the termination of translation
How would you define the different levels of protein structure?
how would you guys define - quaternary and tertiary structure (on an exam paper)
((just want to make sure i've got my definitions correct)
primary = sequence of amino acids
secondary  = formation of alpha-helices or beta pleated sheets
tertiary = formation of function shape of protein due to disulfide (and other)  bonds
quat = more than one polypeptide chain (eg. Haemoglobin)
The tertiary structure of a protein refers to the overall, three-dimensional conformation of a protein, resulting from interractions between the side-chains of the polypeptide chain. The tertiary structure is maintained by hydrogen bonds, ionic bonds, disulfide bridges, hydrophobic interractions, dipole-dipole bonds, etc.

The quaternary structure refers to a protein made up of two or more polypeptide chains. This is maintained by a lot of the bonds involved in maintaining the tertiary structure.
Is an enzymes active shape a result of its tertiary or quaternary structure?
Is the enzyme's active site a function of the polypeptide's tertiary or secondary structure??

Thank you in advance!
Tertiary structure
What does 5’ and 3’ mean?
On a DNA strand, I know it's double stranded, but what do the 5' and 3' at each end actually mean? Thanks
I made mention of this in a post I made quite a while ago (ctrl + F and search "tiny side note"): A Guide to Success in VCE Biology

The principle is called Directionality. Basically, the 5' end of the DNA strand is designated as such because that end of the strand has at its terminus the 5th carbon in the deoxyribose ring (or ribose ring if the strand is RNA).

5' and 3' are just aspects of a carbon-numbering convention, as with this furanose molecule:
What happens as an enzyme is formed through its primary, secondary and tertiary stages or structural change?
Hi guys, could someone help me on this question please
 Describe what happens as an enzyme is formed through its primary, secondary and tertiary stages or structural change. Discuss the structure of the molecule, final shape, and the parts of the enzyme critical to its function. 
Primary structure:
When dabbling into this, the first thing to remember is that enzymes are actually protein molecules. Thus, they are made up of amino acid sub-units linked by peptide covalent bonds. It is the specific, linear sequence of these amino acids that forms the primary structure of an enzyme. Moreover, it is this primary structure that ultimately determines the molecular conformation of the protein molecule (i.e. the enzyme's active site).

Secondary structure:
This is essentially the semi-molecular folding of the protein due to the formation of hydrogen bonds between the peptide bonds. What forms is one of three shapes: random coiling, alpha helices and beta-pleated sheets.

Tertiary structure:
This refers to the overall, three-dimensional conformation of the enzyme (protein). Essentially, it is the tertiary structure that creates the shape of the active site. This region is essential in an enzyme's activity. Obviously, this is due to the fact that the active site is shaped specifically complementary to the shape of a specific substrate.

Things to note:
* Due to the strong covalent (peptide) bonding, the primary structure remains unaffected by denaturation.
* Because the secondary and tertiary structure are maintained by more weaker bonds that are easily disrupted by denaturation, they are affected by this process. As a result, active site configuration is altered, preventing enzyme-substrate complexes form, causing a decline in enzyme activity.
Why aren’t lipids polymers?
hello everyone  ;)
i'm a newbie here and i'll probably ask more questions especially over the summer holidays.. so please take care of me...haha.
anyways, first question, why are lipids not considered a polymer? i can't find a clear answer. And I know they don't have monomers, but i was taught that fatty acids and glycerol were their subunits. What exactly is the difference between a monomer and a subunit then?

Thanks in advance :D

We'll look after you, no fear ;)

Well, a polymer is a chain of repeating subunits - kinda like a necklace, with a string of beads.  But lipids are a bit more like earrings - for instance, triglycerides (fats and oils) have a glycerol backbone and then three fatty acid tails dangling off it.  See how it's not a repeating pattern, a long line (like in proteins, where it's a chain of amino acids, or nucleic acids, where it's a chain of nucleotides)?  --> Not a polymer, and the individual subunits aren't monomers.  That's just how polymer/monomer is defined.
Why is nitrogen essential for life?
random question: why is nitrogen considered to be an essential element for all living things?
Nitrogen is found in amino acids. Amino acids make up protein and protein is used everywhere. Without protein, we wouldn't have enzymes or even RNA polymerase which is essential in protein production. Proteins are very very important.
Also found in nitrogenous bases and some carbohydrates
Why are complementary base pairs complementary?
I have a question. Why are complementary bases complementary?
adenine and thymine share two hydroen bonds, whereas cytosine and guanine share 3. So compatability is the answer, I suppose :)
To add to this: basically adenine and thymine are structured in such a way that they can form two hydrogen bonds, whereas guanine and cytosine are structured in such a way that they can form three. In other words, the pieces of the puzzle just fit together. Adenine and guanine, for instance, can bond to each other, but it's just not as efficient as with their complementary pairs.
Why does RNA have complementary bases given it is single stranded?
Hi, I just had some questions is anyone could help me...
1. For RNA, my teachers have always told me that the complimentary base pairs are A-U and C-G but how can they have pairs when it's single stranded? Like it doesn't have another strand to pair with?
1. During transcription they base pair to DNA
Are there proteins that only have primary or secondary structure?
3. Can a protein that stops at secondary or tertiary structure, or even primary structure (can it stop there?) be considered complete?
3. A protein can't stop at a level of structure. All proteins have primary, secondary and tertiary structure. These structures are just a description of the shape of a protein at any given point (or its amino acid constituents in the case of primary structure). A protein can't be without shape
Why is the primary structure unaffected during denaturation?
Why is the primary structure unaffected during denaturation? And what can actually break down the primary structure? Thanks :)
Peptide bonds are stronger than hydrogen bonds (which can break down during denaturation). Enzymes can break down the primary structure.
Just to add to above response, if you continue to heat a mixture, for instance, one would expect the peptide bonds to break too. In the biological world though, this rarely, if ever happens.
Why does pre-mRNA need to be modified?
    Hi :)

    I was reading the bio notes and it says:

    "The pre-mRNA is modified in three ways:
    • -Segments of the pre-mRNA are spliced and removed from the pre-mRNA and the remaining pieces joined together. The spliced and removed pieces are called introns and the pieces that remain and are joined together are called exons.
    • -A methyl cap is added to the 5' end of the RNA strand.
    • -A poly-A tail is added to the 3' end of the RNA strand."

    I'm just a bit confused as to why the pre-mRNA needs to be modified in the first place, aka why segments of the pre-mRNA are spliced and removed etc. (from the first bullet point). I also don't quite understand the other two bullet points either. Would someone be able to explain this in more depth?

    Thanks so much :D
Pre-mRNA needs to be modified:
1. to remove segments of mRNA that are "non-coding" - in a region of DNA, not all of it is necessary for that particular protein to be made and thus areas of it (called introns) are removed. This is called splicing. Splicing basically allows one sequence of DNA/RNA to code for various proteins depending on how it has been cut up.
e.g. if pre-mRNA has the sequence ABCDEFG
splicing may result in:
ABDFG creating protein type 1
ABCEG creating protein type 2
ACDEF creating protein type 3
This can be really helpful considering that we needs heaps and heaps of different kinds of proteins for all the different cells in the body but we only have so much DNA (about 2 metres in length apparently) :P

2. the mRNA has a poly-A (i.e. lots of Adenines) added to its tail end (3' end) and has a methyl (technically 7-methylguanosine - but not needed for vce) cap added to the "head" end of the strand (5' end). This capping and tailing allows the mRNA to be more stable (i.e. prevents enzymes from degrading the RNA strand) and thus assists it during its "transportation" from the nucleus to the cytosol. (imagine if enzymes were able to degrade the RNA as it moves to the cytosol, no protein would ever be successfully made) The cap and tail also allows translation to be more efficient (how... i'm not too sure sorry  :-\ )
Hope that helps :)
What is meant by the genetic code being universal?
Can someone tell me the most simplest answer that will owe me let's say 1 mark on what makes the genetic code universal?
the same four nitrogenous base pairs ? idk if you could mention structure/ having the same nucleotides, as it may vary [i think] - but generally the same four nitrogenous base pairs in DNA (A,T,C,G)
All organisms use the same nucleotide bases. HasibA is correct :)

On the same page, wouldn't they have to have the same nucleotides as well? I thought the bases were the only variable part (other than deoxyribose sugar vs ribose sugar).
They would indeed
What is meant by redundant and universal?
What are redundant and universal DNA codes? Questions come up on every exam from the past couple of years but I still don't know what it is?
Thanks :)
Universal: all known organisms share the same four nucleotide bases (A.T.G.C)
Redundant: there are 20 amino acids and 64 possible codons, so more than one codon can code for one amino acid.
Why does mRNA have to be synthesised 5’ to 3’?
Hey guys,

Could someone please explain to me why mRNA has to be synthesised in a 5' end to 3' direction?
The 3' end of a nucleotide has a hydroxyl (OH) functional group. Hence nucleotides can only be added to the 3' end of a pre-existing nucleotide since condensation polymerisation requires a hydroxyl functional group so the polymerase enzyme can create a covalent bond between the nucleotides.
What happens during translation?
Could someone please give me a concise summation of 'translation' specifically the part where the tRNA comes into play, I take too long to state it in short answer questions  :(
- Post-messenger RNA (mRNA) binds to ribosome and is read two codons at a time from 5' to 3'
- Transfer RNA (tRNA), with an anti-codon complementary to an mRNA codon, arrives at the ribosome with a specific amino acid
- Amino acids form peptide bonds between each other and form a polypeptide chain

This is about as concise as I can make it...
Feel free to make any corrections ^^
What does a protein folding look like?
When a protein folds, does it literally just... fold? In half or something? Sorry for the weird question, I'm just having trouble visualising the process :-\
I didn't listen to the content of this video, but towards the end it shows an animation of a protein folding.
https://www.youtube.com/embed/yZ2aY5lxEGE

Proteins don't really fold in half as you've described. It's more like origami. A series of deliberate, smaller folds that all conspire to make an exact structure. That's how protein folding works, in essence :)
How should we define mRNA?
3) When defining MRNA, should we mention that "MRNA carries a copy of a segment of genetic code of DNA from nucleus to ribosome" or just mention that it "carries a copy of a segment of genetic code of DNA to the ribosome," VCAA definition in one exam mentioned nucleus but I was thinking that bacteria don't have a nucleus yet they still do transcription involving MRNA?
3) It would depend on how the question is worded. In VCAA exams I doubt they would just ask you to define it without context. If your context has a nucleus then mention it if they're talking about a bacteria then don't. In bacteria its sort of like the ribosomes find the mRNA not so much the other way around. It can end up being translated whilst it is still attached to the DNA and being transcribed - This is why bacterial DNA doesn't have introns.
Do we need to know how polypeptide chains produced at free ribosomes are folded into intracellular enzymes?
When polypeptide chains are produced at free ribosomes, how, are they "converted" into intracellular enzymes? Would it just be post-translation modifications and do we need to know about these (it was referred to in the 2017 examiners report)?
It’s not really converted. An enzyme is just a protein with a specific structure. There are molecules (enzymes I think) that fold the polypeptide into its tertiary shape. I’m pretty sure that’s all you need to know. What specifically did it say on the examiners report?
Well it wasn't relevant to the above, but the multiple genes leading to multiple proteins questions, but wasn't sure if post-translational modifications could result in an enzyme:

2017 VCAA Q1. c):
• different post-transcriptional modification or modifications of the pre-mRNA
• different exons are joined or alternative splicing
• different nucleotide sequences/mRNA sequences, code for a different protein
• post-translational changes to the protein; for example, alternative folding

Since vcaa referred to post-translational modifications, would it be wise to go through it?
nah you definitely don't need to know how protein folding occurs or any other post translation modification occurs.
Yeah definitely not examinable - it would not be the only possible answer to a question. I suspect for this question you would have just had to mention it not talk about it in detail.
What are the levels of protein structure and what type of bonding do they use?
Just wondering how many different levels in the structure of proteins can be identified and their names? Furthermore what are the main types of bondings being involved in the primary structure, secondary structure and also the tertiary structure.
Four levels of protein structure are possible - primary, secondary, tertiary, and quaternary.



The primary structure of a protein is its amino acid sequence.
Amino acids are covalently bonded together into polypeptide chains by peptide linkages.

The secondary structure of a protein requires hydrogen bonding.
There are two basic types of secondary structure:
The (alpha) helices and the (beta) pleated sheets.

The tertiary structure of a protein is formed by folding and bending.

The strongest links holding a folded polypeptide in place are from the bonds between neighbouring cytesine amino acids, which form disulphide bridges.

Other interactions folding the polypeptide include ionic bonds - which can form between positively and negatively charged side chains, hydrogen bonds and hydrophobic interactions.

:)
Do I need to say which direction pre-mRNA is synthesised in?
When describing transcription and translation, do we need to say that pre-mRNA is synthesised in the 5' to 3' direction?
Yes. You can word it differently depending on how you write it but you need to include it somewhere.
Does RNA polymerase break the DNA strand open?

can we say RNA polymerase breaks the dna strand open?
It would probably be better to say that transcription factors unwind the DNA, but I doubt you'd need to incorporate this into your answer. For example, if a question asks for you to describe transcription, you can simply say that the double stranded DNA is unwound, allowing for RNA polymerase to ....etc
Why is protein function determined by the order of amino acids?
Protein function is determined by order of the amino acids. Why is this the case?
Because the R groups of amino acids are highly specific, therefore, a different order of amino acids may result in different reactions between adjacent/ neighbouring R groups resulting in changes in the way the protein folds => changes 3D structure etc...
What’s the importance of having both fibrous and globular proteins?
What is the importance of having two types of proteins - fibrous and globular?
The 3D shapes of fibrous and globular proteins are rather unique. e.g. fibrous proteins, being longer and more narrow, would have a better function as structural proteins (collagen, keratin), while the round/spherical shape of globular proteins is more suited towards being functional (enzyme, hormone etc.)
Does RNA processing happen in prokaryotes (e.g. bacteria)?
Does RNA processing/post-transcriptional modifications happen in prokaryotes like bacteria? I thought it didn't but some practise exams are saying it does?
Thanks!
Doesn’t happen in prokaryotes. They can actually be being translated whilst the strand is still being transcribed!
What’s the difference between a polypeptide and a protein?
3) What is the difference between a polypeptide and a protein?
3) A polypeptide is a chain of amino acids. A protein can be made of one or more polypeptide chains.
How could the same genetic sequence produce different proteins?
How could the same genetic sequence produce different proteins?
Most likely alternative splicing (there are other ways but that's the one in VCE)
What exactly is the tertiary structure?
What exactly would tertiary structure be? Is it just the overall 3D structure of the protein, i.e going beyond just the secondary structure, but now including the 'deliberate' folds of the protein made in the rER? This seems really confusing as various sources are saying that the tertiary structure is the 3D shape- yet even the molecules that make up the primary and secondary structure (which is just if there are alpha helices and beta pleated sheets present) are 3 dimensional.
Yep it's the 3D shape. Technically everything is 3D, but for the sake of describing it, it's the functional 3D shape of a protein.
The tertiary structure is the 3D shape. I understand your confusion with alpha helices & beta pleated sheets - think of it as further folding. Another way you can distinguish the two (I'm not saying this as a guide for what to refer to in your answers) is that secondary structure is the result of hydrogen bonding, whereas tertiary structure results from a range of different attractions.
How much do we need to know about the structure of DNA and RNA?
With DNA and RNA, is it sufficient to know the similarities and differences, what they are made up of, their condensation polymerisation reactions and that the RNA polymerase binds to the promoter region at the 3' to start reading the DNA template strand? How granular do we need to get regarding the structure of these nucleic acids? (Do we need to know about the diagrammatic representation of nucleosomes to chromosomes and is it required that we understand what distinguishes uracil from thymine? Is this too much?)
You need to know everything you mentioned up to RNA polymerase. You don't need to know about nucleosomes or chromosomes (that's 1/2 content). You don't need to know much about the bases - just which ones can bind to each other and whether they're found in DNA or RNA.
What happens to the mRNA strand after translation?
What happens to the mRNA molecule after translation? Can it be reused by the cell whenever the protein it codes for is needed, or is it that one mRNA codes for only one copy of one protein and then is destroyed or something?
The one mRNA strand can be translated multiple times to produce multiple (identical) polypeptides. The poly A tail that is added during post-transcription modification helps the mRNA strand stay around for a bit. Eventually it gets broken down though - but I don't know exactly how that works (and you don't need to know the details).
Cell's don't want the mRNA strand to stick around for long- otherwise the cell will be wasting energy producing proteins it does not require. Therefore, what it does is that it adds a Poly-A tail to the 3' end during post-transcriptional modificaiton. Not only does this Poly-A tail provide the mRNA strand with stability, but this tail gets shorter and shorter every time a ribsome synthesises a polypeptide chain. So, eventually, the Poly-A cap is completely gone, and then it gets broken down by an enzyme or something (not sure quite how this bit happens). I am almost certain that this is carried out by a protein of some sort however.

Note here that the Poly-A tail is not very long (I believe it to be only about 250 adenine bases long), so it can still get used multiple times and not stick around for too long either. 
What are the differences and similarities between the different types of RNA?
Hi.
I was wondering what the differences and similarities are between the three forms of rna subunits?
Thanks.
I'm going to assume that by "forms of subunits" you are talking about the types of RNA:    tRNA, mRNA and rRNA :)

tRNA - carries a specific amino acid to the ribosome for translation, and it does so as it has a specific anticodon that is complementary to the codon of the mRNA.

mRNA - is the product of transcription - RNA polymerase (enzyme) transcribes the DNA template strand which then results in a sequence of nucleotides complementary to template strand. The nucleotides are ‘read’ by the ribosome three at a time (codons).

rRNA - together with various proteins make up the ribosome.

Essentially, they all play roles in in transcription and translation which is required in order for cells to manufacture proteins (which are responsible for carrying out cell functions that sustain life).

Note: any RNA contains Adenine, Guanine, Cytosine and Uracil (no thymine!)

So similarities:
- they all have A,U,G,C bases

Differences:
- They all play different roles in protein synthesis as mentioned above
- They all have different structures, I’m not quite sure how to embed pictures just yet, but if you google them you will find that mRNA looks like a ‘spring’ or ‘coil’ whereas tRNA has a clover shaped ‘loop’ structure

Last year we were told that we should confidently be able to label and/or identify tRNA and its anticodon and also be able to provide sequences complimentary to any strands of RNA that we were provided with.
« Last Edit: February 27, 2019, 09:44:11 am by PhoenixxFire »
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Re: Biology Q&A archive/Bio FAQ
« Reply #3 on: April 09, 2018, 09:33:43 pm »
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U3 AOS1 Gene structure and regulation
Relevant study design dot points
• the functional distinction between structural genes and regulatory genes

• the structure of genes in eukaryotic cells including stop and start instructions, promoter regions, exons and introns

• use of the lac operon as a simple prokaryotic model that illustrates the switching off and on of genes by proteins (transcriptional factors) expressed by regulatory genes.

What is the difference between gene expression and gene regulation?
gene expression vs gene regulation? explain please,
thanks
Gene expression is the transcription and translation of genes to form a protein. Gene regulation is the switching on and off of genes to ensure that particular proteins are only produced when they're needed.
What are the 3’ and 5’ ends of DNA
My question is what is the difference between the 5' and 3' ends of a DNA strand and more importantly, is this knowledge required for the VCE course?

Thanks in advance.
The 3' is the -OH end and the 5' is the phosphate end. Yes this knowledge is required for the VCE course. You will have to know the direction of replication and transcription of DNA with respects to this configuration.

Here's a good way to remember:

Five - Phosphate (same sound)
Three - Free (no phosphate) (similar word)
What is meant by saying that a hormone alters the expression of a gene?
What is specifically meant by saying hormones act by altering the expression of genes?
To initiate the transcription of a gene, you need to recruit an enzyme called RNA polymerase. There are a number of different ways this can work, but in general, in eukaryotes RNA pol requires a host of proteins to express genes. These proteins are called transcription factors. What an enzyme may do is alter a transcription factor, allowing it to bind. It may also bind itself at a different site.
Why is gene regulation necessary?
Why is gene regulation necessary? I know it's necessary as protein synthesis requires energy, but what else?
Thanks :)
Synthesising proteins unnecessarily wastes energy, like you said. Also, say the gene encodes a protein hormone. We might want that hormone synthesised and secreted only at specific times, say, in development (eg. you wouldn't want the hormones that trigger puberty being produced in an infant). Production and release of a protein may have harmful consequences if inappropriate, which is another reason why gene regulation is important
What is the role of the promotor region?
Role of the promotor region of a gene???
Cheers,  :)
Region that initiates transcription of an mRNA molecule.

This occurs due to a variety of reasons including the attachment of a hormone-receptor complex that attaches to the promotor region of a gene.
What’s the difference between gene expression and gene regulation?
gene expression vs gene regulation? explain please,
thanks
Gene expression is the transcription and translation of genes to form a protein. Gene regulation is the switching on and off of genes to ensure that particular proteins are only produced when they're needed.
Does lactose binding cause the repressor to detach?
Lactose attaches to repressor proteins which this change its shape causing it to detach from the operator region right?
Correct
What’s the difference between structural and regulatory genes?
What is the difference between structural and regulatory genes? Different sources contradict each other so I’m not really sure what VCAA wants us to know
Regulatory genes produce a gene product that is involved in the expression of other genes.
Structural genes produce a gene product that is involved in normal cellular metabolism.
Is RNA polymerase a transcription factor?
Is RNA polymerase technically a transcription factor?
I would say no. Transcription factors alter the rate of transcription, RNA polymerase actually does the transcription. I suppose you could count that as altering it because without it the rate of transcription would be 0 but I’d still say it’s not a transcription factor.

I agree with this. Definitely not a transcription factors. Transcription factors are basically things that help RNA polymerase work (therefore RNA pol itself is not a TF).

U3 AOS1 Structure and regulation of biochemical pathways
Relevant study design dot points
• the role of enzymes as protein catalysts in biochemical pathways

• the mode of action of enzymes including reversible and irreversible inhibition of their action due to chemical competitors at the active site, and by factors including temperature, concentration and pH

• the cycling of coenzymes (ATP, NADH, and NADPH) as loaded and unloaded forms to move energy, protons and electrons between reactions in the cell.

Are ATP/NADPH nucleic acids?
Would ADP/ATP and NAD/NADH be considered nucleic acids?
No, I wouldn't consider them nucleic acids but only because nucleic acids are, by definition, large macromolecules. ADP/ATP is a nucleotide (well for the sake of VCE bio it's probably best to consider it a nucleotide with 3 phosphates instead of one, but I think it's actually considered a nucleoside (nucleotide minus the phosphate) bound to 3 phosphates...) and NAD is a dinucleotide (the D actually stands for Dinucleotide!)
I'd say they're nucleotides but not nucleic acids; nucleic acids are large polymers.
Why does rate of reaction slow down as temperature decreases?
When the temperature goes below optimum, the enzyme reaction slows down (and can even cease.) Is this because the active site of the enzyme has changed conformation or is it because collisions between enzyme and substrate is low?
Thanks
Fewer collisions between the enzyme and substrate molecules
What does it mean when enzymes lower activation energy?
What is it meant by when enzymes lower their activation energy? What exactly is activation energy?

Activation energy (Ea) is the minimum energy input needed for a chemical reaction to occur. All reactions need some energy input to facilitate their occurrence, but the Ea is often too high for biological systems, which are vulnerable to heat and other forms on high-energy situations.

Enzymes are biological catalysts. Catalysts lower the Ea of a chemical reaction system, which means the energy "currency" of the reaction is within more a more manageable range that the biological system (e.g. an organism) can manage without sustaining any damage. Biocatalysis is also important because organisms only have a certain amount of energy that they can devote to biological reaction systems, which means that by lowering the required energy input for vital biochemical reactions, the organism's energy input (such as food) can be reduced.
The effect of enzyme concentration on reaction rate
Regarding Enzymes:
So, IF you assume ample substrate and cofactors present, if you increase the concentration of enzymes, will the rate of the reaction similarly increase in a linear fashion?
I am assuming ideal conditions.

Does the rate of reaction eventually plateau or will the rate of reaction continue to increase assuming the said conditions?
Answering your first question: if you increase substrate concentration as you increase enzyme concentration, the reaction rate of the enzyme will increase in a linear fashion, assuming all other variables are kept constant. However, you may see a plateau because of product concentration, which forms almost an obstacle that limits the time interval in which the enzyme & substrate combine & react together, thereby reducing the activity rate of the enzyme.
So basically, the concentration of product surrounding the enzyme and substrate hinders the formation of the enzyme-substrate complexes-and this accounts for the plateau eventually?
Yes, think of it as "getting in the way" of the reactions
Does a coenzyme effect the amount of product produced?
Would a coenzyme have any effect on the amount of product produced?
If an enzyme requires a coenzyme to interact with a specific substrate, then the presence of that coenzyme would definitely have an effect on the amount of product produced in a given time.
What exactly do enzymes do?
I was a bit confused about the function of enzymes. According to my textbook, enzymes reduce activation energy however have no effect on the rest of the reaction. Is this true? If so, when people say that enzymes catalyse a reaction, do they actually mean that enzymes catalyse the beginning of a reaction?

Thank-you!
It depends on the type of enzyme really. It's hard to explain, because it's kind of true and kind of not. Some enzymes just orient things better, and that reduces the activation energy, whereas others actually press and hold substrates together, and thereby participate in the whole reaction. Just presume that reactions are instantaneous (each individual step that is).
Why can substrate build up stop competitive inhibitors binding but not stop non-competitive inhibitors?
Why is it that competitive chemical inhibitors will stop binding to an enzyme if there is a build-up of substrates?
Why don't non-competitive inhibitors also stop binding?
A competitive inhibitor binds to the enzyme's active site. We can reverse this inhibition by increasing substrate concentration, as the substrate can essentially "overpower" the effect of the inhibitor by occupying the active site instead, in a way 'forcing' the inhibitor out of the active site (remember that the enzyme in this scenario is specific to both the substrate and the competitive inhibitor).

Non-competitive inhibitors do also stop binding (I think you may have made a small error in the question :) ), but this form of inhibition is not considered reversible (within the bounds of the VCE curriculum) because the inhibitor binds to a site OTHER than the active site. This distorts the shape of the enzyme's active site, which means that increasing substrate concentration will have no effect because the substrate cannot bind to the active site.
What does it mean that an enzyme is an organic catalyst?
Enzymes are also called 'organic cataylsts.' What is the meaning of this term?
Basically, they speed up chemical reactions by lowering its activation energy (initial amount of energy required to kick start the reaction). ' Organic catalyst' is the same as 'biological catalyst', essentially.
Definition of enzyme denaturation
hii,
Whats an accurate definition for enzyme denature that would be awarded full marks on the exam??
The image one is a definition to a question in the insight exam about denature exam. it seemed my own definition lack a bit of information to it and had more of other stuff, so i was just wondering what would be an specific one to answer on VCAA exams?
thanks.
Enzyme denaturing occurs when the enzymes is exposed to high temperature, more that it's optimum range which then cause the active site of the enzyme to change shape. This restricts the enzyme from performing any more reactions as no substrates can bind to it anymore. Someone pls correct me if I'm wrong. Just saying this from the top of my head. :)
My definition was something like enzyme denature is an organic catalyst which has its specific tertiary structure conformation shape altered, hence loses its ability to accommodate previous substrates and thus loses its function (guessing I need to also talk about hydrogen bonds braking due to heating, anything else) thanks
This sounds good, but I think you should mention how an enzyme denatures at high temperatures (H bonds breaking) as well somewhere in your response.
Denaturation is when temperature or pH deviates from a predefined optimum level such that intermolecular bonding in the protein is disrupted, changing the 3-dimensional conformation of the protein. It is an irreversible process and results in a loss of function.

Important points that have been missed

-irreversible
-pH can do it as well
The things you need to know for VCE is that it's irreversible. When you scramble an egg, you denature the protein. You can't "unscramble" an egg, it is permanently like that. It's a great example to remember. That's the key concept they actually want you to remember in my humble opinion. AS T-Rav said, both heat and pH (less sensitive to this though) can do it. If you look at in terms of the lock and key model, you're essentially changing the shape of the lock. Imagine if i came to your house and changed every lock or the shape of your power points, nothing would work, the keys wouldn't go in and your plugs wouldn't go in, things just fall apart and fail to function.

Spoiler
Recent research has suggested denaturation might not be permanent in some cases and enzymes can partially "refold" and regain some functionality, in particular smaller ones. Not relevant for VCE though.
   
Temperature/pH needed to denature an enzyme?
There was lots of confusion on this topic, so I’ll give you my explanation instead:
pH Extreme pH at either end of the scale will denature enzymes, if you draw a graph to show this, it will be symmetrical.
Temperature Lower temperatures will not denature an enzyme, they just slow everything down, reducing interaction between the enzyme and substrate, which lowers the rate of reaction. Each enzyme has an optimal temperature (human enzymes are around 37 degrees Celsius) When this temperature is exceeded, the rate of reaction slows down, as the substrate/enzymes are moving too fast to work properly. As the temperature is increased you hit a point where the enzymes denature (called the critical temperature). If you need to discuss when denaturation due to temperature occurs say ‘Enzymes (proteins) denature when the temperature far exceeds the optimum temperature.’
Factors affecting enzyme activity/rate of reaction
Can someone please concisely explain the factors affecting enzyme activity/rate of reaction? Cheers :)
pH- Can change enzyme shape by changing the charge on amino acids. Can also denature Enzymes at extremes.
Temperature- Kinetic energy causes molecules to move around faster. At a low temp, the molecules (enzyme/substrate) move more slowly and thus, lower rate of reaction. At a higher temp, the molecules move around faster so there are more collisions. However, if the temp increases above the optimum, enzymes will dentaure permanently.
Substrate concentration- Reaction rate increases with increasing substrate concentration. There is a limit to this increase however - once all active sites are occupied (saturated), adding more substrate will not increase the reaction rate
Enzyme Concentration-  As the enzyme concentration increases the rate of the reaction increases linearly, because there are more enzyme molecules available to catalyse the reaction. At high enzyme concentration, the substrate becomes the limiting factor so the reaction rate becomes constant.
Do the factors that affect enzymes apply to all proteins?
Do the factors that affect enzymes apply to all proteins?
Not all. Factors such as increasing substrate concentration don't really have an effect on structural or fibrous proteins. Factors such as pH and temperature do. However, not all proteins have an optimum temperature or pH like enzymes do, and so will not be affected in this regard.

EDIT: I didn't read the your question properly the first time, so I fixed up my answer now C:
Proteins that aren't enzymes seldom do anything. They normally are something rather than do something. So no. Anything relating to functionality is irrelevant when talking about other proteins.
What happens to enzymes at very cold temperatures?
What happens to enzymes at very cold temperatures? I know their ability to catalyse reactions is reduced but is it because they do not have enough energy to faciliate the reactions or because their shape is changed temporarily (or neither)?
Its because at low temperatures the kinetic energy is greatly decreased so therefore reactions will occur really slowly.

When an enzyme is inactive, molecular movement is so slow that the substrate barely makes contact with the active site (hence on temperature  enzyme activity graphs, it starts at 0)

EDIT: spelling, wrote this too fast :P
This is part of it, but not all of it. It means that the proportion of molecules that have activation energy sufficient enough to cause the reaction is lower, because that's what temperature is a record of, the kinetic energy of a system. So it's not that they're not making contact, they are, that contact just isn't forceful enough to supply the energy needed to start the reaction.
Does adding more enzymes/substrate increase the product or the rate of reaction?
I'm a tad confused about enzyme activity/rate of reactions.

When you are increasing the substrate or enzyme concentration, does this mean you are generating more product or just decreasing the time it takes to get to a certain amount of product?
If you increase the amount of enzyme, you increase the rate of reaction, but do not end up with more product.
If you increase the amount of substrate, you increase the rate of reaction (up to the saturation point, where it plateaus), you do end up with more product.
What is the optimum range of an enzyme
Can someone please define 'optimum range', in terms of enzymes?

Because I thought this was a bit different between the definition of the optimum range, we learnt for abiotic factors in Biology Units 1/2.

Is this true?

Thanks! :)
I'll attempt this:
Optimum range is the specific environment range in which an enzyme works best. This so called "environment" may be temperature, pH etc. So there is a specfic range in which an enzyme best functions at
Pls correct me if I'm wrong
Do inhibitors stop enzyme activity or reduce it?
Would it be correct to say that inhibitor molecules, stop enzyme activity altogether?

Or do they only decrease it?

Thanks!
Permanent inhibitors stop enzyme activity altogether. Temporary inhibitors slow down the reaction from occurring.
When referring to a single enzyme, competitive inhibitors stop it, non-competitive slow it down. When referring to multiple enzymes, competitive inhibitors may not bind to every enzyme, so it could just be slowed down (due to less enzymes available to catalyse reactions), not stopped entirely.
How do enzymes speed up chemical reactions?
can somebody elaborate on how enzymes speed up chemical reactions? Like what happens with the chemical bonding etc
Enzyme catalyse or speed up chemical reactions by lowering the activation energy of the reaction. They achieve this by influencing the stability of the bonds within the reactants; in anabolic reactions, they facilitate the formation of the product by essentially binding the reactants together, while in catabolic reactions, they facilitate the breakdown of bonds within the reactant.
Are all catabolic reactions exergonic and all anabolic reactions endergonic?
Is it correct to say that all catabolic reactions are exergonic and all anabolic reactions are endergonic?

Thanks!
Yes
Are metabolic pathways and biochemical pathways the same thing?
Do extreme pH’s cause enzymes to denature?
With enzymes, do extremes of pH cause the denaturing of the enzyme?
Yes, extremes in pH do cause enzymes do denature. The majority of eznymes will denature with pH 2 or less (except Pepsin), and denature with pH 12 or more. High temperatures may also denature enzymes.
Can the products of enzyme-mediated reactions act as a non-competitive inhibitor of the enzyme?
Can the products of an enzyme-mediated reaction act as non-competitive inhibitors of the enzyme?
Feedback inhibition is normally non-competitive.
What is an allosteric site?
What is an allosteric site?
An allosteric site is a site on an enzyme other than it's active site. In some cases the binding to an allosteric site can activate the enzyme while in other scenarios the function can be inhibited.
Why are enzymes/cofactors so important in biochemical reactions?
Why are enzymes so important in biochemical pathways?

Why are cofactors important in biochemical pathways?
Enzymes are required to lower the activation energy of metabolic reactions/processes, hence speeding up the reaction process - without enzymes an organism's metabolism would be too slow.

Cofactors are required for some metabolic reactions as the enzyme alone will not catalyse the reaction. In many cases the addition of a cofactor forms the shape of the active site for substrates to bind to.
What is the purpose of the NAD+ molecule?
What is the purpose of the NAD+ molecule?
It's an unloaded carrier molecule. It is loaded with H to form NADH. NADH is then unloaded to form ATP in the electron transport chain, releasing NAD+ back for reuse.
Why does the rate of reaction slow down when temperature decreases?
When the temperature goes below optimum, the enzyme reaction slows down (and can even cease.) Is this because the active site of the enzyme has changed conformation or is it because collisions between enzyme and substrate is low?

Thanks
Fewer collisions between the enzyme and substrate molecules
What is Pi?
Hello,
can someone please explain what the Pi is?
The Pi is a phosphate group. ATP has 3 while ADP and 2.
Pi is an inorganic phosphate, it is the product when you break down ATP into ADP + Pi. ATP has three phosphates where as ADP has 2. ATP is usually broken down into ADP + Pi to release energy where as ADP is attached to Pi to form ATP which is then broken to release energy.
What’s the role of inhibitors on regulating enzyme activity?
can someone help me with this question?
state the role of inhibitors in regulating enzyme activity?
Firstly enzyme inhibitors are molecules that bind to an enzyme in which they subsequently block the active site in a competitive way leading to a decreased enzymatic activity. The binding of an inhibitor stops substrate from entering the active site, thus hindering the enzyme's activity/rate from catalysing the given reaction. In doing so, the enzyme's activity is regulated in correspondence to the concentration of inhibitors present.
Does increasing substrate concentration overcome both types of inhibition?
Does increasing substrate concentration overcome both types of inhibition?
Nope. Only overcomes competitive inhibition. Noncompetitive inhibition changes the active site so it doesn't matter how many substrates there are
Nope. Only overcomes competitive inhibition. Noncompetitive inhibition changes the active site so it doesn't matter how many substrates there are
Do enzymes speed up the rate of reaction?
Question about enzymes:

If enzymes reduce the activation energy require for a reaction to initiate, does this mean that comparing it to a reaction without the enzyme, that it would occur at a rapid rate, that is, the product/s will be released faster than usual?

Im also not getting my hear around enzyme concentration and how it can affect the rate of reactions.

Any help is greatly appreciated, thank you.
Without the enzyme the reaction would take a lot longer to reach the activation energy required for the reaction to continue, hence the rate of reaction (products released) will be incredibly slow, too slow to sustain life. With enzymes this activation energy is lowered so the reaction takes less time to proceed to completion.
The more enzymes you have the faster the rate of reaction will be as there is an increased chance that the substrate will bind to the active site of an enzyme and be turned into product. However continuing to add enzymes does not continue to increase the rate of reaction, after a certain point, adding enzymes will no longer increase rate of reaction ( the rate of reaction won't increase due to other factors like not enough substrate, temperature etc.)

I really hope this made sense, ask if there's any part that confused you :)
What are inhibitors and why are they used?
What are inhibitors? And why are they used?
Inhibitors are any  molecules or competing substrate the binds to the enzyme and decreases it's activity. The inhibitor may either bind to the active site (preventing the substrate from binding to the active site) or bind to another part of the enzyme (called the allosteric site), which deforms the shape of the active site so it's unable to bind to the substrate and catalyse the required reaction.

Drugs are the most common type of inhibitors. Some drugs inhibit enzymes that are required for pathogens to survive.

There's also different types of inhibition like reversible and irreversible inhibition but these should be outlined in your textbook
What’s the difference between a cofactor and a coenzyme?
Can someone explain Cofactor vs Coenzyme

A cofactor is any inorganic substance, such as an ion, that assists an enzyme in it's function, whereas a coenzyme is any substance, but is organic, and activates the enzyme, hence allowing it to function.

Do enzymes denature at low temperatures?
What happens to enzymes at low temperatures? Do they denature like they do at extremely high temperatures?
Hey

Enzymes will not denature at very low temperatures but their activity will be heavily reduced due to the decrease of average kinetic energy at low temperatures. Once heated back up to optimal temperature the enzyme will continue to function as there is no permanent damage like there is to the 3-D shape(tertiary structure) when the enzyme is heated.
How do extreme temperatures and pH denature enzymes?
Also, HOW do extreme temperatures and pH denature an enzyme?
Enzymes are proteins that have very specific shapes. Altering the shape in anyway can potentially (and usually) stop the enzyme from being able to function. The tertiary structure of a protein consists of bonding between the side chains of the amino acids, extreme heat allows these bonds to be broken, changing the shape. When cooled down it is improbable that the bonds will reform in the exact same way before the heating, rendering the protein useless.

pH can also break the bonds that hold the side chains together, again disrupting the structure. Simply reversing the pH again is improbable to return the protein back to its original shape.
What are cofactors and coenzymes? What’s the difference?
What is a cofactor and what is a coenzyme? How are they related? Are they organic? What are some common examples of each?

Thanks in advance
Cofactors and coenzymes are substances that are needed to be present for the enzyme to catalyse a reaction. They generally bind loosely and temporarily to a specific enzyme which allows it to perform its biological function. Cofactors are usually inorganic minerals and ions while coenzymes are usually organic vitamins.
Are coenzymes reusable?
does anyone know if coenzymes are reusable? one book says they are but one says they arent!!
Coenzymes are reusable. Common coenzymes include ATP, NADH, and NADPH :)
What’s the point of cycling through NADH/ATP?
What is the purpose of cycling between NADH and NAD+, ATP and ADP and NADP+ and NADPH?

I am more so confused about how to phrase my answer, but it would have to do with the fact that reusing molecules allows for conservation of energy.

Thanks

The hydrogen ions need to be broken off anyway (eg. To power ATP synthase in cellular respiration) and the phosphate needs to be broken off to release energy, so there’s no point throwing away the unloaded molecule you end up with.

I don’t know exactly what sort of answer you are after (it depends on the question) but if you’re being asked why they are recycled I would just say something like:
Unloaded carrier molecules are reused by the cell as it is faster than making new molecules and it conserves resources and energy.

What is the role of substrates and enzymes?
Hi all! Just one question:
I can't quite seem to grasp the concept of substrates and their role with enzymes? Could someone please explain the role of substrates and enzymes?

The enzyme catalyses (instigates) a reaction. The substrate is the thing that the reaction happens to (it is just a molecule - any molecule that binds to an enzyme can be called a substrate). Enzymes place a little bit of force on substrates, forcing them to change in one of two ways. They either:
-Cause bonds holding the substrate together to break, resulting in 2 or more products.
-Cause bonds between 2 or more substrates to form, resulting in 1 product.

Without enzymes it would take far, far longer and more energy, for the substrate to change (for a chemical reaction to occur). Imagine 2 substrates just floating around in your cell. Without enzymes it is highly unlikely they will ever fuse together, however an enzyme is able to bond to them, holding them against each other in the correct place to allow bonds to form.

The enzyme stresses (places pressure on) the bonds, which is explained by the induced fit theory - this says that when substrate/s bind the enzyme changes shape slightly.

(Image removed from quote.)

Are cofactors required for some reactions?
Are cofactors a requirement for certain enzymes, or do they simply increase the rate of a reaction?

Technically the enzymes themselves are not required but obviously the reaction would be extremely slow without them.

So yes cofactors are required, the reaction could happen without them but not at any useful rate.

Can reactions occur without enzymes? How?
How can reactions occur without the presence of enzymes, such as starch to maltose in presence of amylase?

Is it just due to natural collisions between substrate molecules; how would product formation work if it was not lock and key/induced fit?

Also, can all reactions occur without enzyme presence, its just that these reactions would occur too slowly?
So enzymes decrease the activation energy of a reaction thus making the reaction occur at a much faster rate. By removing enzymes, the reactions can indeed still occur, however of course they would be way too slow to be able to maintain life. The binding of the substrates to an active site for product formation would simply decrease the activation energy to bind them together - so therefore without enzymes, they would solely rely on collisions, but would be very slow as the activation energy is significantly higher. As for starch to maltose without the presence of amylase, the enzyme decreases the activation energy to break the bonds, so without enzymes, it would just take much longer to reach the required activation energy etc.
Why are enzymes important for cellular processes?
Hi! Does anyone know how are photosynthesis and enzymes linked?? and why are they important as part of key cellular processes of the cell?? Thanks! :)
Cellular reactions can't* occur without enzymes. In photosynthesis a large number of chemical reactions are needed (called a biochemical pathway) to build glucose. Pretty much every cellular process needs enzymes to catalyse the reactions that allow them to occur.

*Well they can but it’s too slow to sustain life
Is there a functional difference between coenzymes and cofactors?
is there a functional difference between coenzymes and cofactors?
I don't believe that there are really any significant functional differences that you need to know for VCE, after all, coenzymes are a subset of cofactors - they're just organic. So any function of a coenzyme would ultimately come under a function of a cofactor. But I suppose that one off the top of my head would be that coenzymes can act as carrier molecules i.e. they can carry electrons/protons between reactions etc, and other cofactors just increase the rate of a reaction - they increase the affinity of the enzyme for its substrate (the ease with which the enzyme binds to the substrate)
Your first sentence in this is really excellent, capturing the meaning of both really well.

Just for interest, cofactors don't actually just increase the affinity for a substrate. Indeed, this is not usually how they function. They actually tend to act as temporary electron donors and acceptors (hence the reason they're metals!)
How does a repressor stop transcription?
When the repressor protein binds to the operator region, does RNA polymerase still bind to the promoter region but it just can't move across the structural genes?

Or would it be better to say that the repressor protein blocks RNA polymerase from binding to operator region?
The repressor which binds to the operator, hence blocking RNA polymerase from binding to the promoter region
Does it really block it from binding to the promoter region though? Cause the repressor protein binds to the operator, which is on the right of the promoter. So isn't it more correct to say that the repressor prevents it from moving along the structural genes?
Well at a VCE level, I'm pretty sure that you can just say that because the repressor binds to the operator blocking RNA polymerase from binding to the promoter, therefore it is unable to move along the structural genes.
Does translation occur in the cytoplasm or at ribosomes?
Does translation occur in the cytoplasm or ribosomes? Which is preferred as an answer?
ribosomes should be enough.

Saying ribosomes in the cytoplasm discounts translation occuring in the RER so just saying ribosomes would be more appropriate.
Is enzyme optimal temperature an example of natural selection?
Is enzyme optimal temperature an example of natural selection?

- so only organisms with correct enzyme optimal temperature survived, reproduced, passed on favourable alleles to offspring

Am I overthinking this or would this be correct?
Purely speculation, but given the importance of enzymes I'd imagine that a mutation that resulted in an enzyme functioning less efficiently would probably result in the death of that individual. So in a way yes it would be natural selection. Probably not something you'll ever have to talk about for VCE though haha
Is competitive/non-competitive inhibition always reversible/irreversible?
2) Is competitive inhibition always go with reversible inhibition, and non-competitive irreversible?
2. For VCE, yes.
« Last Edit: November 27, 2018, 02:16:11 pm by PhoenixxFire »
2019: B Environment and Sustainability/B Science @ ANU

PhoenixxFire

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Re: Biology Q&A archive/Bio FAQ
« Reply #4 on: April 09, 2018, 09:34:39 pm »
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U3 AOS1 Cellular respiration
Relevant study design dot points
• the purpose of cellular respiration

• the location of, and the inputs and outputs of, glycolysis including ATP yield (details of the biochemical pathway mechanisms are not required)

• mitochondria as the site of aerobic cellular respiration, an overview of their structure and evidence of their bacterial origins

• the main inputs and outputs of the Krebs (citric acid) cycle and electron transport chain including ATP yield (details of the biochemical pathway mechanisms are not required)

• the location of anaerobic cellular respiration, its inputs and the difference in outputs between animals and yeasts including ATP yield

• factors that affect the rate of cellular respiration, including temperature, glucose availability and oxygen concentration.

Where does the energy to make ATP come from?
Where does the energy to make ATP from ADP+Pi come from? Since it's an anabolic reaction.
Breaking down sugars, fats etc. Because they release energy, the break down of them is used to fuel the reaction between ADP and inorganic phosphate.
Oxidative phosphorylation, which is the formal term for what Vox Nihili mentioned above.
Why does ADP have to add another free phosphate before it can break off the terminal phosphate to release energy?
Just curious why does ADP have to add another free phosphate molecule before it can brake of the terminal phosphate to release energy. Why isn't ADP capable of also breaking of its terminal phosphate??
It technically could, and in some reactions it does. It's just that ATP is better set up to do it. I can't exactly explain why, because it'd require higher level chemistry than I'll ever know, but it'll have to do with ATP—>ADP just being an easier pathway to cycle through, and give the biggest energy yield as well. It's also probably because AMP is also a nucleotide, so ADP—>AMP levels wouldn't be able to regulated as well as ATP/ADP :)
Why is ATP needed in glycolysis?
In glycolysis, why is ATP needed? The breakdown of glucose is catabolic, therefore energy releasing (exergonic), so where in glycolysis do anabolic (endergonic) reactions occur?

Also, why is H2O produced?
If you think about it, to start a fire you need a spark. That spark produces a tiny fire, that let's the fire go. Undeniably, the overall process of burning all the wood though produces a lot more heat than the spark. Likewise, every reaction needs a spark like that, it's called its activation energy. ATP supplies that spark. It supplies a tiny bit of energy to get the reaction going, then that reaction is able to release a lot of energy itself.

Just the groups that react. There are a couple of protons and an oxygen spare, so they make H2O
Why is glucose the main source of energy in cells, rather than lipids?
Why don't cells use lipids instead of glucose as the prime reactant in cellular respiration, since it yields more energy?
Cellular respiration is just one energy generating process. There are a host of different energy sources that are actually used by body cells. Sugars are certainly one, but they're not the only, as you know. Indeed, there are cells that don't use glucose (or any sugar) at all to generate energy. Glucose is just a handy energy source because it can be involved pretty well with a lot of biochemical pathways. It's just sort of convenient, easy to obtain in the environment, easy to break down and transport. One particular disadvantage of having lipids as the prime energy source would be that they can't really be transported via blood that well, they're not soluble. That's probably the big issue with them really. :)
What happens to NADH molecules that are loaded during glycolysis of anaerobic respiration?
I was wondering about the fate of the NADH molecules in anaerobic respiration. When the net 2 ATP is produced, and NAD becomes loaded to NADH, what happens to the NADH after that. Surely, they can't get unloaded right, because there's no more ATP produced in that process?
I'll try this:
Are you talking about glycolysis? If yes, I think that when the pyruvate breaks down to form lactic acid (humans), it needs the hydrogen ions from the NADH. So the hydrogen ions and the breaking down of pyruvate, makes lactic acid/ ethanol and CO2. Then the NADH become NAD and the process begins all over again.
Cellular respiration described in words?
Could someone please explain cellular respiration in the easiest terms possible?
All the arrows in the diagrams and the values of the inputs and outputs are really confusing me :(
Much appreciated ;D
This topic felt so much easier when things were kept simple, so I'll try outline what I gathered from it all (:

Cellular Respiration can be of two types: Anaerobic or Aerobic.
Anaerobic respiration occurs in the absence of oxygen, whereas Aerobic respiration requires the presence of oxygen.
In glycolysis, 1 molecule of glucose is split into 2 molecules of pyruvate in the cytosol. This process requires 2 ATP, but yields 4 ATP (hence the net yield is 2ATP).  NAD is loaded to NADH for each molecule of pyruvate (so you actually end up getting 2 NAD being loaded to 2NADH). Glycolysis is required for both anaerobic and aerobic respiration.

In Anaerobic respiration, the carrier molecules (NADH from glycolysis) are used to produce 2Ethanol & 2CO2 molecules in plants or lactic acid (2 molecules of lactate) in animals. Note that the two pyruvates which were produced in glycolysis are considered the inputs in this stage. Anaerobic respiration itself does not yield any ATP, although the 2ATP netted in glycolysis should be considered.

Aerobic respiration occurs in the matrix of mitochondria, and is coupled to the electron transport chain (which occurs in the cristae of mitochondria). After glycolysis has occurred, a 'link reaction' takes place to form an intermediate product (2C) that combines with a 4C compound (or 'respiratory substrate') to enter the Kreb's cycle. The Kreb's cycle removes carbon from this 6C compound (or 'respiratory substrate') in stages, which is let out as carbon dioxide. One 2C has been removed as carbon dioxide (meaning the substrate is now 4C) it combines with the 2C intermediate product at the start of the cycle, allowing the cycle to start all over again! During the Kreb's cycle certain electron carriers (NAD and FAD) are loaded with Hydrogen to form NADH and FADH2, and there is a net yield of 2ATP as well.
In the electron transport chain, these carriers unload their Hydrogen ions. The Hydrogen ions flow through a pump(s) in the cristae producing energy in the form of ATP. This produces 32 or 34 ATP.

I'm not going to write out the whole equation as that's kinda pointless I think, but know that it was formed by just adding all the reactants of the process on one side and the net yields of all the products on the other side.

That's basically it. I've skipped over lot of the technical speak as books contain so much of it already. I've also skipped lots of numbers and amounts of stuff, but unfortunately this is something you've probably got to memorise.
Why are the products of anaerobic respiration different in plants and animals?
Why do the products of anaerobic respiration differ between animal and plant cells?
I think it's because of the the fact that there are different enzyme pathways in animal and plant cells which result in different products (lactic acid in animals, ethanol and carbon dioxide in plants/fungi)
Anaerobic respiration is used by few microorganisms which use an inorganic acceptor like Sulfur and does not utilize oxygen or pyruvate and derivatives of pyruvate. Depending upon the end product anaerobic respiration is of two types:

Glucose→ 2 ethanol + 2CO2 + 6ATP

(alcohol is the product; commonly occurs in plants like yeast)

Glucose→ 2 lactic acid + 2ATP
(animals)
How do you remember the inputs and outputs of cellular respiration?
How do you guys manage to remember the inputs and outputs of photosynthesis and cellular respiration?
You might want to try visualise the situation and then input any missing links.

For example, the Light-Dependent Stage of Photosynthesis:
-Light energy (I) splits the Water (I) molecule
-Think "Okay, splitting means energy is released, ATP (O). Oh, but then this requires ADP + Pi (I ) to be made.
-Think "The remaining Hydrogen forms NADPH (O), but to do so thus needs NADP (I)

So, basically remember two main components from each section, and you should be able to do the above. Just try to picture where each substance would go, what it needs to create it, and the like. To continue on, then Light-Independent, the NAPDH must combine with the CO2 to produce Glucose. This requires energy, so ATP is input, thus ADP+Pi output. The hydrogen ions were given, so output is NADP.

However, it may be easier for you to just rote learn the inputs and outputs. Try to repeatedly say the inputs and outputs for each section, then cover to test yourself. Maybe even writing it out each time may be useful for you to remember.

Hopefully this helps :)
Do we need to know how many of each product is produced per molecule of glucose?
Do we need to know how many of each product is produced for one molecule of glucose in aerobic respiration?
Yes there are always questions on that even if it is MC
Which stage of aerobic respiration is oxygen actually used for?
Aerobic respiration is the breakdown of glucose in the presence of oxygen. In which stage, out of the 3, is oxygen actually involved in?
Oxygen is used up in Electron transport. The hydrogen ions carried by NADH and FADH are combined with oxygen to synthesise water.
Why is it advantageous to convert pyruvate to lactic acid?
Question I came across in a practise exam

What advantage does an animal cell gain by converting pyruvate to lactic acid. Explain

Thanks
The conversion requires the oxidation of NADH to NAD+. In turn, the process frees up the number of NAD+ available to be used in glycolysis, so that this latter process can continue (not indefinitely, however). Recall that glycolysis produces a net of 2 ATP and 2 NADH per glucose (edit: also 2 pyruvate).
Also it is faster than aerobic respiration.
How are the outputs of cellular respiration produced?
How are each of the outputs of cellular respiration produced?

Thanks in advance:)

Cellular respiration:

In cellular respiration, glucose is broken down into 2 molecules of pyruvate in the cytosol of cells and the process is known as glycolysis. This process does not require oxygen to proceed. Once the glucose is broken down, 4ATP molecules are produced and 2 molecules are reused for the reaction, and so 2 molecules are transferred to the next stage of cellular respiration, where oxygen is a necessity. The two molecules of pyruvate enter the mitochondrion, where they react with CoA to produce Acetyl CoA. This reaction produces one molecule of NADH, and so two molecules of pyruvate will produce two NADH. The Acetyl CoA molecules will now undergo the krebs cycle, where they will undergo several reactions to produce 1 molecule of ATP each, 3 molecules of each as well as 1 and 3 molecules of NADH. This will result in 8 molecules of NADH and 2 molecules of ,   and 2ATP per molecule of glucose. The carbon dioxide is released at this stage and this whole process of reactions was accomplished in the mitochondrial matrix. The 'carriers' transfer to the cristae (the inner membrane of they mitochondria) where the electron transport chain occurs. The final acceptor here will by oxygen, to accept the hydrogen ions that are left unused and will form water as a result. There will also be a production of 32-34 molecules of ATP during the ETC. So we previously had a production of 2ATP (in glycolysis), 2ATP (in krebs cycle) and now 32-34 ATP. In total: 36-38 ATP.

I hope this helped you xD

Overview of cellular respiration?
can anyone please explain cellular respiration?
Cellular respiration is the process whereby unicellular and multicellular organisms convert chemical energy (glucose, sugars, more complex carbs) into a form of energy that cells can rapidly and conveniently use, the form known as Adenosine Triphosphate (ATP). Now in VCE biology, glucose is the main sugar that is known to be hydrolyzed for energy harvesting.

Glycolysis:
What happens?
Glucose molecules are broken down via enzymes.

What is released?
- 2 pyruvate molecules
- 2NADH molecules
- 2 ATP molecules (however there are 4 produced in total, but 2 are used up in the same reaction, so net production of 2).

Where does it occur?
Cytosol of cells.

Does it require oxygen?
No. If there is no oxygen available after glycolysis, then the pyruvate molecules will undergo fermentation reactions, in animals lactic acid is produced, and in plants/yeast ethanol and CO2 are produced. However, if there is oxygen available in the cell, then the following reactions will also occur after glycolysis.

Krebs cycle (Citric acid cycle):
What happens?
In the Krebs cycle, the two pyruvate molecules enter the mitochondria to undergo further reactions. There are two minor stages (not formal) in the krebs cycle, an initial stage where the pyruvate molecules react with CoA (coenzyme A) to produce CO2, NADH and Acetyl CoA. The Acetyl CoA then undergoes further reactions and produces another two CO2 molecules, 3 NADH molecules and 1 ATP molecule and 1 molecule of FADH2. Remember that two molecules of pyruvate are yielded from 1 molecule of glucose.

What is released?
- 6CO2
- 8NADH
- 2FADH2
- 2ATP

Where does it occur?
Krebs cycle occurs in the mitochondrial matrix (the fluid substance that is enclosed within the inner membrane of the mitochondria)

Does it require oxygen?
Yes, hence this is the second step of aerobic cellular respiration, and the following process is the final step of the aerobic pathway.

Electron Transport Chain:
What happens?
Remember the 'carrier' molecules from the previous pathways? Well the NADH and FADH2 molecules move along to the cristae of the inner membrane (projections of the inner membrane) and they release their electrons and H ions. The electrons 'flow' along the protein molecules embedded within the cristae (known as cytochromes). As these electrons pass along the cytochromes, the hydrogen ions are also being released from the NADH molecules. This means that a concentration gradient is accumulating of H ions, hence the Hydrogen ions need to diffuse (facilitation, since ions are charged and cannot simply diffuse through the membranes) down their gradient. As this occurs, the transmembrane (a protein that is embedded and protrudes through the membrane) enzymes known as ATP synthase simultaneously synthesise ATP molecules as Hydrogen ions diffuse down. This process synthesises approx. 32-34 molecules of ATP, depending on the need and type of cell (muscle cells require 34 as they are involved in more movement and protein contractions as compared to the cells of the stomach). So what happens with the hydrogen ions and the electrons that are being passed down the various cytochromes? Well, lone oxygen molecules await them and accept them, to produce water (H2O).

What is released?
- 32-34 ATP molecules
- 8NAD+ (no need to list this)
- 2FAD (no need to list this)
- Water molecules (amount not required)

Does it require oxygen?
Yes and it is the last step of aerobic cellular respiration.
Why do some cells produce more ATP per glucose than others?
1. Why do some cells produce 36 ATP via aerobic respiration while others produce 38? (Some sources say that the extra 2 ATP comes from glycolysis while others say that it comes from the electron transport chain)
1. In some cells the ETC is more efficient than others, hence the difference. I highly doubt that it's because of different ways of doing glycolysis.
How many ATP are produced during the electron transport chain?
Exactly how much ATP molecules are produced in the ETC? Which is better to write- 32 ATP molecules or 36-38? I'm super confused
1. 32-34, the other four come from glycolysis and Krebs
How does the electron transport chain work?
Can anyone explain the electron transport chain to me in simpler words?
NAD+ and FAD drop off electrons and protons --> electrons are passed along proteins embedded in the membrane --> this allows protons to be transported across the membrane --> Proton gradient is created --> Protons move through a special enzyme embedded in the membrane called ATP synthase --> as protons move through ATP synthase it drives the production of ATP --> Oxygen is the final electron acceptor

Note:
Proton = H+ ion
Is pyruvate or acetyl-coA the input for the Krebs cycle?
hi!
you know for the krebs cycle, there's a step before it known as the intermediate step. Do we include that as part of the krebs cycle for the exam or pretend it doesnt exist? like should i write pyruvate as an input for krebs or acetyl-coA? and should i write 4CO2 produced or 6?

Thank you! :)
Excellent question, and one of the odd things about the course. I think you’d probably get away with either pyruvate or acetyl-CoA to be perfectly honest. Likewise with the CO2
How do limiting factors work?
Just need help clarifying a few things. Can anyone explain how the limiting factors(main ones that we're expected to know about) affect photosynthesis and cellular synthesis.

What are your thoughts on it? It's easier for us to help you if you try your hand first :) I'll give one example and explain my process, then you can try applying it to other ones. We can help from there

1: Pick a limiting factor -- I've chosen to use CO2 concentration in photosynthesis
2: What does this factor do? -- CO2 provides carbon to make C6H12O6
3: What would decreasing this do? -- If there was less CO2 available, then there would be less carbon available. If there is less carbon available, not as much glucose can form. This decreases the rate of production.
4. What would increasing this do? -- If there was more CO2 available, there would be more carbon available for glucose to form. Provided the other necessary ingredients are there, this would increase the rate of glucose production until it begins to plateau. Do you know why this plateaus?

You can apply this to anything. As long as you know what each factor does, you can work out how it is limiting. Please note that the limiting factor is whatever there is least of. It doesn't matter if you have all the CO2 in the world if you don't have any light, or vice versa. Hope this made sense/was helpful :)

Why can’t fermentation go on indefinitely?
Explain why yeast fermentation cannot go indefinitely?

I know that lactic acid fermentation will result in muscle fatigue (which is why it doesn't go indefinitely), but not sure about yeast fermentation.

Fermentation produces ethanol and carbon dioxide. If there is sufficient glucose, the yeast will continue to undergo fermentation until the accumulation of ethanol kills it because ethanol is toxic.

Is Acetyl Co-A or pyruvate the input for the krebs cycle?
Just wondering in regards to the Kreb Cycle if we should say that the pyruvate molecule or acetyl coenzyme A is used as an input?

Thanks heaps!
Well the correct answer would be Acetyl CoA because the pyruvate is converted into Acetyl CoA prior to entering into the krebs cycle

You should be fine with using either. Technically the input is acetyl co-A but a lot of people won't be taught that because the details of krebs have been removed from the study design.

I've had a quick look through past examiners reports:
2016: Pyruvate is referred to as a substrate of the kreb's cycle
2010: "• Krebs (cycle): pyruvate is converted to carbon dioxide, 2 ATP produced "
2017: "The structure labelled Y is where: D. pyruvate is broken down, releasing carbon dioxide"

I only found one reference to acetyl coA and it was talking about details that are no longer on the study design. So I would just go with pyruvate but you should be fine to use either.
What’s the difference between an acceptor molecule and a carrier molecules?
Hey all,
Could someone please give me the definition of an acceptor molecule in layman's terms?
Are they different to carrier molecules?
Thank you!!
Acceptor molecules are basically those which accept/receive other particles such as protons (hydrogen ions), electrons etcetera. I suppose you could say that they are technically "carrier molecules" for example, NADP+ accepts electrons and protons to form NADPH and is hence a carrier molecule. And the final electron acceptor in the electron transport chain in respiration is Oxygen, which combines with the electrons and hydrogen ions to form water - which I suppose you could call a carrier molecule, as it provides the electrons/protons needed in the light dependent reactions in photosynthesis
Okay, thank you so much! That makes sense now. <3
So, would you then say that FADH2 is or isn't an acceptor molecule?
I've never learnt much about the difference (or lack of) between them but I would just stick with carrier molecule because that is what VCAA uses in the study design.
FADH2 would not be an acceptor molecule as it is already it its loaded form so it acts as a donator, instead of acceptor. FAD would be an acceptor as it accepts electrons/protons to form FADH2
How much detail do we need to know about Krebs cycle?
Do we need to know the stages of the Calvin Cycle in detail? Is there a diagram that presents just enough information for the VCE level or are the diagrams on Google what we are supposed to memorise?

Thank you very much!
Nah, you don't need to know the Calvin cycle in detail. Just that CO2 is fixated/reduced into glucose would suffice and then touch on the other outputs/inputs and location of course.
You don't need to know any details at all. CO2 goes in, glucose comes out.
This is part of those biochemical pathways that have been removed from the study design, you may still see it appearing in tests up to 2016 though.

Edit: Beaten by darkdzn. Damn you are fast :P
What are the exact inputs and outputs of each stage of cellular respiration?
Hey guys,

What are the inputs and outputs of the three stages of aerobic respiration (glycolysis, krebs cycle, electron transport chain)?
I've read my textbook as well as online, but the exact number of molecules are different.
Also, how much ATP is produced by the ETC and aerobic respiration as a whole? I have heard that there is disagreement over the number of ATP produced.

Thank you! ;D
Hey
So for the exact numbers of inputs/outputs of the various stages does have some discrepancies between different sources so if you want to memorise them, then memorise the ones that your teacher gives you.

Glycolysis
Input: Glucose, NAD, ADP +Pi
Output: Pyruvate, NADH, 2ATP

Krebs Cycle
Input: Acetyl CoA (or pyruvate however there is actually a transition stage which converts the pyruvate into Actyl coA prior to entering into the krebs cycle), ADP +Pi, FAD, NAD
Output: CO2, 2ATP, FADH2, NADH

Electron Transport
Input: NADH, FADH2, ADP+Pi, O2
Outputs: NAD, FAD, 34ATP, H2O

So 2+2+34 = 38 ATP produced in total
However, of course, in reality this ideal 38 ATP produced is not always the case as the cell can "lose" pyruvates or possibly expend more energy in adverse conditions etcetera. Despite this being said, in past VCE exams, I've seen that they've generally accepted a range of answers e.g. 36/38. NOTE: DO NOT write 36-38. VCAA does not like ranges. Use EITHER 36 OR 38. Although it is best to just stick with whatever your teacher tells you
These are the exact numbers I used:

Glycolysis:
C6H12O6 + 2ADP + 2Pi + 2NAD+ = 2 pyruvate + 2H2O + 2ATP + 2NADH

Krebs cycle:
2 Pyruvate + 2 ADP + 2 Pi + 8 NAD+ + 2 FAD = 6CO2 + 2 ATP + 8 NADH + 2 FADH2

Electron transport chain:
6O2 + 10 NADH + 2 FADH2 + 32 ADP + 32 Pi = 6H2O + 10 NAD+ + 2 FAD + 32 ATP

but as darkdzn said you definitely need to know the exact number of ATP, you might need to know the number of NAD, you don't need to know the number of FAD

The ATP difference is because 2 are used up in cellular respiration, and some cells (e.g. muscles) are more efficient so they make more. You can use either 36 or 38 - it doesn't matter.
Is ATP an input of glycolysis?
Is ATP an input of Glycolysis? Google tells me that an input of glycolysis is 2 ATP for an output of 4 ATP (net gain of 2 ATP). Is this true?
Yes, you are correct - ATP is an input of glycolysis

Yep, but just ignore it for VCE bio.

That’s the 2 ATP that causes variation in what people say the ATP output is. For VCE the study design says that you need to know the net output.
Is more carbon dioxide absorbed in photosynthesis than is released in cellular respiration?
Is more carbon dioxide absorbed in photosynthesis than is released in cellular respiration? And if so, why?
Well this would ultimately depend on the rate of photosynthesis vs rate of respiration, so at times, it can indeed be a greater intake of CO2, while at other times there is an equal uptake or lower uptake. There would be a greater intake when the rate of photosynthesis exceeds the rate of respiration. There would be an equal uptake when the rate of photosynthesis equals the rate of respiration - this is also known as the compensation point. And when the rate of respiration exceeds the rate of photosynthesis, then there would be a lower uptake. The lower uptake may be due to other limiting factors e.g. light intensity etc affecting the rate of photosynthesis
What’s the difference between lactate/lactic acid and pyruvate/pyruvic acid?
in my textbook certain words are used interchangeably:

- "lactate" and "lactic Acid"
- "Pyruvate" and "Pyruvic Acid"
my teacher says that lactate and lactic acid is the same thing, as with pyruvate and pyruvic acid.
is this true?
I'm asking this because during anaerobic respiration in mammals, the textbook says the output is lactate
 
There is a minor technical difference between the two, however for VCE, you can just assume they’re the same thing :)
Does the rate of photosynthesis affect the rate of aerobic respiration?
Hey guys,

Does the rate of photosynthesis affect the rate of aerobic respiration?
Thanks!
I suppose it could affect it if there was very little glucose (produced by photosynthesis) present to act as an input for aerobic respiration. It wouldn't happen naturally, but I suppose you could set up the conditions so that a slow rate of photosynthesis meant few inputs available for aerobic respiration (e.g. closed system with all oxygen coming from photosynthesis).
How many water molecules are produced in the Electron Transport Chain?
how is it that 6O2 molecules can enter the electron transport chain, and 6H2O molecules be produced

it seems that 12 oxygen atoms go in, and only 6 come out.

??? ???
12H2O come out, but 6H2O are used as part of the reaction. So we just cancel out the 6.
What’s the purpose of the hydrogen ion concentration gradient in the ETC?
- in electron transport chain, I understand that hydrogen ions are transferred from NADH and FADH2 to create a hydrogen ion concentration gradient, but what is the purpose of this gradient?
I think that it's so that the hydrogen ions have a high concentration so they want to move out, and move through the ATP synthase which creates energy to turn ADP,P into ATP.
You want to create a H+ gradient (a "proton gradient") across the inner mitochondrial membrane where H+ is higher in the intermembrane space (the space between the inner and outer mitochondrial membranes) and lower in the matrix. You create that by pumping H+ into the intermembrane space from the matrix - this is an energy-dependent process (using energy of the electrons provided by NADH and FADH2).

Once you have a H+ gradient across the inner mitochondrial membrane, H+ will move down its gradient (from the intermembrane space back into the matrix) through ATP synthase. This movement of H+ through ATP synthase provides the energy ATP synthase uses to generate ATP from ADP and Pi.

This is beyond the scope of the course, though - just know your inputs and outputs, and site, and maybe just that ATP synthesis in this step requires a proton gradient created using electrons from NADH and FADH2 :)

Why is the Krebs cycle considered aerobic respiration when it doesn’t require oxygen?
Why is the krebs cycle apart of aerobic respiration if it does not require oxygen?
Here is just my logic (but someone else will explain better):
- without oxygen, NADH can't be converted back to NAD in ETC. So there is no NAD for Krebs cycle
- ATP has to be used to make more ATP, so if 32 net ATP isn't produced in ETC (as a result of no oxygen present), then there is less ATP to carry out specific reactions (such as Krebs Cycle)

Hopefully that's right.
Ok, so the order of the reactions is:
-Glycolysis
-Kreb's Cycle
-Electron Transport Chain

In Glycolysis, we don't need oxygen. However, for the pyruvates to move into the mitochondria, the presence of oxygen is required. So, even though the later 2 reactions might not directly need oxygen, the cell needs to have oxygen for the reactions to continue.

Hopefully that makes sense.  :)
Why is oxygen required for pyruvate to move into the mitochondria?
Why is oxygen required for pyruvate to move into the mitochondria?
Apologies to any Chem students reading this explanation, but a simple way to think about it is that the reactions that occur in the mitochondria eventually lead to the electron transport chain.
Kreb's produces all of your loaded carriers (i.e. NADH, FADH2) which then go to the ETC, offloading electrons and hydrogen ions. Those electrons are then "accepted" by oxygen, which takes them away.

If there weren't oxygen, then the electrons in the ETC would have nowhere to go. If the electrons have nowhere to go, the ETC gets clogged up. If the ETC is clogged up, the carriers can't offload. If the carriers can't offload, you don't make any new NAD+. If there's no NAD+ Kreb's reactions can't occur. If Kreb's can't occur, then the pyruvate in the mitochondria doesn't get used. If the pyruvate doesn't get used, it builds up in the mitochondria. Once it's built up, the mitochondria stops bringing in more pyruvate (because it's already got too much).
« Last Edit: November 27, 2018, 02:16:57 pm by PhoenixxFire »
2019: B Environment and Sustainability/B Science @ ANU

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Re: Biology Q&A archive/Bio FAQ
« Reply #5 on: April 09, 2018, 09:37:06 pm »
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U3 AOS1 Photosynthesis
Relevant study design dot points
• the purpose of photosynthesis

• chloroplasts as the site of photosynthesis, an overview of their structure and evidence of their bacterial origins

• inputs and outputs of the light dependent and light independent (Calvin cycle) stages of photosynthesis in C3 plants (details of the biochemical pathway mechanisms are not required)

• factors that affect the rate of photosynthesis, including light, temperature and carbon dioxide concentration.

Concise explanation of photosynthesis
Also could someone please post a concise explanation if possible of photosynthesis according to what needs to be actually known in the scope of the VCE course?

I would be greatly appreciative.
Photosynthesis occurs in two stages:

Light-dependent stage:
1.) This stage takes place in the thylakoid membranes of chloroplasts.
2.) Light energy is absorbed by chlorophyll molecules; electrons within chloroplasts become energised.
3.) Water is split to form H+ ions and oxygen gas.
4.) NADPH and ATP is formed.

Light-independent stage:
1.) This stage takes place in the stroma of chloroplasts.
2.) Carbon dioxide reacts with H+ ions (provided by NADPH) to produce glucose.
3.) ATP provides the energy for the synthesis of glucose.
4.) Excess H+ ions react with O2- ions to produce water (a by-product).
Light-Dependent Stage:
- Chlorophyll molecules absorb light energy.
- Electrons in the chlorophyll molecules become excited; as a result, the excited electrons enter the electron transport chain.
- To replenish the electrons lost from chlorophyll molecules, water is split to form H+ ions and oxygen gas (a by-product).
- NADPH is formed from NADP+ and H+ ions.
- ATP is formed from ADP + Pi (i.e. Adenosine Di-phosphate + Inorganic phosphate).

Light-Independent Stage:
- Carbon dioxide reacts with H+ ions (provided by NADPH) to form glucose. ATP provides the energy needed to synthesise glucose.
- After the electrons travel through the electron transport chain, they are collected by oxygen atoms, which then become O2- ions. O2- ions then react with excess H+ to form water (a by-product).
Chloroplast structure
Hi is the inner membrane of the chloroplasts what makes up the thylakoid membrane?
Or is the thylakoid membrane a third membrane of itself?
Because I read two different pieces of information from two different sources and so I was confused!
Thanks :)
(Image removed from quote.)

A chloroplast has an inner and outer membrane. The space within the inner membrane is referred to as the lumen of the chlorplast and is filled with a fluid called stroma. Within this lumen there are grana, which are stacks of these membrane-bound structures called thylakoids. The membranes of these thylakoids are called the thylakoid membranes (which makes sense :P). Thylakoids are hollow, and that hollow space within them is called the thylakoid lumen

The light-dependent stage of photosynthesis occurs on the thylakoid membranes
Are 6 or 12 water molecules needed for photosynthesis?
With regards to the reactants of photosynthesis, is it more correct to say that there are 12 molecules of H20 as opposed to 6 (considering both equations are balanced)?
You can use either! I personally opted for the 12 H2Os
If they ask for the net input per glucose molecule I'd say six
I always got told to put 12 on the left hand side and 6 on the right hand side, due to the fact that two separate stages are occurring in which 12 water molecules do react and 6 are produced per glucose molecule.
How does temperature effect photosynthesis?
Does temperature affect how much CO2 is taken in and how much water is lost in photosynthesis?
For water, I'm assuming yes because of transpiration??
Can the Calvin cycle (light independent reaction) only occur in the dark?
Can the Calvin cycle can occur only in the dark?
Nope that would mean that plants only have 'dinner' :P
But yeah, the Calvin cycle can also occur in broad daylight, the only reason why it is called the 'dark-reaction' is because unlike the 'light-reaction', the Calvin cycle does not need an input of sunlight.
How do light intensity/chlorophyll concentration/oxygen concentration affect photosynthesis?
How does light intensity, chlorophyll concentration and oxygen concentration affect photosynthesis?
Increasing light intensity = more light available to the plant (more electrons in chlorophyll molecules can be excited at any point in time) = greater rate of photosynthesis. Eventually you'll reach a point though were increasing light intensity further has no effect on the rate of photosynthesis (if you've got a graph of the rate of photosynthesis this corresponds to a plateau)

Greater chlorophyll concentration = more chlorophyll molecules available to absorb light at any point in time = greater rate of photosynthesis

Increasing oxygen concentration may increase the rate of photosynthesis slightly, but probably only if the plant was in an environment depleted of carbon dioxide. Increasing O2 concentration would increase the rate of aerobic respiration in the plant, increasing the rate at which CO2 is produced by aerobic respiration. If we increase this rate of CO2 output the plant is more rapidly able to use that CO2 for photosynthesis (as part of the light-independent stage). Most likely though the plant will have a plentiful supply of CO2 from the atmosphere, so this increase in CO2 output from aerobic respiration will have only a negligible effect on the rate of photosynthesis
How do the light dependant and light independent stages of photosynthesis work?
how does the light dependent and light independent stage in photosynthesis work? The textbooks seems confusing can someone explain it an easier way?
I'll try to explain it in a more detailed way:
Light dependent stage:
Plants contain chlorophyll in their leaves, when they are exposed to sunlight, light energy will excite the electrons in the chlorophyll and these exited electrons are what trigger photosynthesis.

Firstly, photosynthesis can be seen as a reverse of cellular respiration in which light dependent stage occurs in a slightly similar fashion as the Electron transport chain in respiration. What's different is obviously the location of light dependent stage, which is in the thylakoid membrane (grana). Embedded in these thylakoid membrane are protein channels and enzymes that are able to produce ATP. Excited electrons will release the energy that it gains from sunlight to these protein channels and that will be used to actively pump the H+ ion out of the outer space membrane to generate a concentration gradient. When we have a sufficient concentration gradient between the inner cell and outer space membrane, H+ ions will flush back into the ATP syntheses for the production of ATP ( at this stage, you can see that it is exactly like Electron transport chain). However, the H+ ions will be shuttled by the electron carrier called NADP+ ( whilst cellular reparation is NADPH). Moreover, referring back to what happened with the chlorophyll, since it has donate some of its electrons to the protein channels, it is now electron short, and immediately need some source of electron to make up for this. This is why H20 comes into need, water will be split into H+ ion and O2 due to the high electronegativity that chlorophyll proceeds. O2 will be released out of the plant cell through stomata.

Hence, what we end up after the light dependent stage is a lot of ATP, NADPH and O2 (O2 is a by-product).

Light-indenpendent stage (Calvin cycle):
Now that we have produced a lot of ATP and NADPH, let's make some glucose. Cells use the energy from ATP to combine the H+ ion that NADPH brings and CO2 into glucose. This process in called Carbon fixation in which we are changing Inorganic carbon into Organic Carbon. Notice that we adding simple structure molecules into a complex structure, this is called anabolism ( hence it is endergonic and also a condensation process). What we get after joining molecules together? H20. This is when the RHS H20 in the equation comes from. It is worth notice that the LHS H20 and RHS H20 are not the same because one is used and one is newly formed.

Hence, what we end up after the Calvin Cycle is Glucose ( C6H12O6), NADP+, ADP + Pi, H20.
Hope this helps!
Simple description of the Calvin cycle (light independent reactions
could somebody explain the calvin cycle in simple terms? :)
During the calvin cycle, the NADPH molecules from the light dependent stage of photosynthesis react with 6CO2 to synthesise glucose. At the same time, 6H20 is produced.

This stage which is also known as the light independent stage of photosynthesis is driven by the energy (18 ATP molecules) that is produced in the light dependent stage of photosynthesis.

So basically:
The inputs are: 6CO2 + 18ATP + NADPH
And the outputs are: C6H1206 + 18ADP + 18Pi + 6H20
How is photosynthesis the opposite of cellular respiration?
Can someone explain to me the process of cellular respiration in simple terms, and how exactly it is the opposite of photosynthesis? Also this is a bad question but when plants photosynthesise glucose, do the glucose molecules then go through cellular respiration?
Ok, to start off: cellular respiration is the process by which cells break down sugars to create useable energy sources. It takes place in the mitochondria (hence them sometimes being referred to as the 'powerhouse' of the cell) and needs oxygen to occur.
Represented as an equation, cellular respiration looks like this:
C6H12O6 + 6O2 -> 6O2 + 6CO2 + Energy (ATP)
This can be resented in a worded equation as:
Glucose + Water -> Oxygen + Carbon Dioxide + Energy (in the form of ATP)
ATP or adenosine triphosphate has three phosphate groups attached and when it releases one, it also releases energy and the remaining molecule is now called ADP or adenosine diphosphate.

For your second question (cellular respiration = photosynthesis?) my answer is that they are both the same on a chemical level, and are simply reversed ( as photosynthesis is represented as: 6O2 + 6CO2 ----> (using sunlight energy) C6H12O6 + 6O2). also photosynthesis are also rather opposite in that they occur in different organelles (photosynthesis occurs in the chloroplasts), a catalyst is needed for photosynthesis (chlorophyll) but not for cellular respiration, photosynthesis is anabolic, whereas cellular respiration is catabolic, they (as already shown in the chemical equations) do opposite things with oxygen and carbon dioxide; photosynthesis turns carbon dioxide into oxygen and  cellular respiration turns oxygen into carbon dioxide.
So theoretically, if we put an organism which uses cellular respiration (all animal cells do) into a sealed, glass jar with a plant that photosynthesises (most do, although onion, for example, doesn't) then they could actually live together if also equipped with water sunlight food, ect.   how cool is that?!
However, they are not exactly opposite, because although they are reversed chemical equations, they are not reversed processes (for example, at no point does cellular respiration require sunlight for an energy source). 

And for your third question, the glucose produced by photosynthesis is sometimes used for cellular respiration, although it may also be converted to sucrose and then transported around the plant for other uses, i.e. sweetening the fruit of the plant or it may be stored as starch for later needs (including cellular respiration)

Hope I helped :)
tl;dr no, just read it, too hard to explain any shorter :P
Why do leaf discs float when they photosynthesise?
In the experiment of photosynthesis, why does the leaf disc float when it photosynthesises?

The leaf disc is initially sunk because the oxygen was sucked out of it, making it more dense than the solution in which is sits in. So when it's placed in a beaker, and as it photosynthesises, oxygen is produced as the H20 is broken down by chlorophyll. When this oxygen is produced, it is either released in the atmosphere or stored in the spongy mesophyll of the leaf discs, hence the discs start to float again as they become less dense than the solution in the beaker.

Hope it helped :)
How are the outputs of photosynthesis produced?
How are each of the outputs of photosynthesis produced?

Thanks in advance:)
Photosynthesis:

So you can see that glucose, oxygen gas and water are all products of photosynthesis. Firstly, water is absorbed by the plant and the chlorophyl pigments located on the thylakoid membranes (grana) of the chloroplasts of photosynthetic leaves absorb sunlight, this sunlight is then used to split molecules into it's constituent particles: Hydrogen, oxygen and electrons. The oxygen binds with another oxygen molecule that undergoes the same pathway, and forms oxygen gas. This oxygen gas is released into the atmosphere. The hydrogen ions and electrons are then carried by carrier molecules called NADP+ forming NADPH, ATP is also formed as a result. The NADPH and ATP leave the thylakoid membranes and now are surrounded by the stroma of the chloroplast. Here they will undergo the light-independent reactions of photosynthesis, where they are used to break down carbon dioxide obtained from the atmosphere into glucose. Note that the unused hydrogen ions of the light-independent reactions that are not used to make this conversion, are joined with oxygen and produce water, as a by product and this is why sometimes you do not see water a part of the outputs os photosynthesis, because it will basically be reused. Same goes with ADP + Pi and NADP+ after they 'deliver' the electrons and hydrogen ions to the light-independent stage, they will be reused again in the light-dependent stage and hence are not represented in the equation.

I hope this helped you xD

What is the role of NADPH & ATP in photosynthesis?
Im currently undertaking VCE 1 & 2 biology and was wondering if any of you guys would be able to help me with the role of NADPH in photosynthesis? and then a separate question to that is what is the purpose of ATP, ADP and Pi in photosynthesis? thank you so much in advance.
NADPH 'carries' a hydrogen atom as well as electrons to the light-independent reactions that occur in the stroma, and these are consumed there to produce the final product of glucose. That is all you need to know about NADPH. ATP is synthesised during the light-dependent stage. Basically, ADP + Pi come along, and they are bonded together to form ATP. This ATP molecule is the universal energy source for many organisms. So this is used to drive, provide energy for the light-independent reactions.
Why does the krebs cycle stop if oxygen is not present?
2. Why is it that if oxygen is not present, the Krebs cycle (as well as the electron transport chain) comes to a stop?
2. Because NADH/FADH2 aren't being used by the ETC, this feeds back and halts their production by the Kreb's cycle. Not necessary to know this in VCE though, of course and it is a little more complicated than I've explained, but this should do.
How do limiting factors work?
Just need help clarifying a few things. Can anyone explain how the limiting factors(main ones that we're expected to know about) affect photosynthesis and cellular synthesis.

What are your thoughts on it? It's easier for us to help you if you try your hand first :) I'll give one example and explain my process, then you can try applying it to other ones. We can help from there

1: Pick a limiting factor -- I've chosen to use CO2 concentration in photosynthesis
2: What does this factor do? -- CO2 provides carbon to make C6H12O6
3: What would decreasing this do? -- If there was less CO2 available, then there would be less carbon available. If there is less carbon available, not as much glucose can form. This decreases the rate of production.
4. What would increasing this do? -- If there was more CO2 available, there would be more carbon available for glucose to form. Provided the other necessary ingredients are there, this would increase the rate of glucose production until it begins to plateau. Do you know why this plateaus?

You can apply this to anything. As long as you know what each factor does, you can work out how it is limiting. Please note that the limiting factor is whatever there is least of. It doesn't matter if you have all the CO2 in the world if you don't have any light, or vice versa. Hope this made sense/was helpful :)

What level of detail do we need to know about photosynthesis? Do we need to know the number of molecules?
Hello,

What is the level of detail required for VCE Biology Units 3 and 4 regarding photosynthesis?
Also, do we need to know the number of molecules (inputs and outputs) for both photosynthesis and respiration?

Thank you very much everyone. :D
You just need to know the inputs, outputs, location (and a bit about chloroplasts) and factors that affect the rate of photosynthesis (e.g. temperature)

Yes you need to know the exact number of molecules, however you don't need to know the number of ATP produced in photosynthesis (but you do need to know how many are produced in each stage in respiration).

Study design dot points
Photosynthesis
• the purpose of photosynthesis
• chloroplasts as the site of photosynthesis, an overview of their structure and evidence of their bacterial origins
• inputs and outputs of the light dependent and light independent (Calvin cycle) stages of photosynthesis in C3
plants (details of the biochemical pathway mechanisms are not required)
• factors that affect the rate of photosynthesis, including light, temperature and carbon dioxide concentration.

When it refers to the purpose of photosynthesis, you just need to understand that oxygen is just a waste product, and that the glucose is intended to be used by the plant in its own cellular respiration.
For the actual processes, you just need to know the inputs, outputs, location and a general idea of what is happening in each stage - your level of detail doesn't need to be deep at all. For example, if the question asks you to describe what is happening in the light dependent stage or something along the lines of that, you generally just need to say

- Occurs in Thylakoid membrane of the grana
- Light energy is captured by the chlorophyll and used to split a water molecule
- Splitting provides electrons and hydrogen ions which are accepted by NADP+ to produce NADPH
- The splitting also produces oxygen which diffuses out as a byproduct
- ATP is produced from ADP +Pi (You can add in that ATP Synthase is the enzyme which catalyses this, but you don't need to know that)

Edit: Beaten by PhoenixxFire but I'll post it anyways :P

What does NADP do in the light dependant stage?
slightly confused

can someone please explain NADP's role in the light dependant stage of photosynthesis.
cheers
So NADP+ acts as an electron acceptor (or electron carrier) in the light dependent stage of photosynthesis. Thus, it "accepts" or "carries" the hydrogen ions and electrons released from the splitting of the water molecule to form NADPH.
Minor detail
It accepts electrons from the dependent stage, and donates them to the light independent stage.
It’s a pretty cool process.
What stage of photosynthesis does changing light intensity effect?
Hey again! I just want to make sure I've got this right, so I understand that as light intensity increases so does the rate of photosynthesis and if there's too much light it reaches a light saturation point. But if there's too little light that means the light-dependent stage won't be able to take place. For CO2 concentration it also reaches a certain point where the enzymes are saturated, but I'm not sure what stages it would affect and how.
CO2 is an input of the light independent stage so it would effect that. Both light intensity and CO2 concentration (and all other limiting factors) would actually slow down both reactions though as the light independent stage requires products from the light dependant stage and the light dependant stage needs the NADP+ from the light independent stage.
Is more carbon dioxide absorbed in photosynthesis than is released in cellular respiration?
Is more carbon dioxide absorbed in photosynthesis than is released in cellular respiration? And if so, why?
Well this would ultimately depend on the rate of photosynthesis vs rate of respiration, so at times, it can indeed be a greater intake of CO2, while at other times there is an equal uptake or lower uptake. There would be a greater intake when the rate of photosynthesis exceeds the rate of respiration. There would be an equal uptake when the rate of photosynthesis equals the rate of respiration - this is also known as the compensation point. And when the rate of respiration exceeds the rate of photosynthesis, then there would be a lower uptake. The lower uptake may be due to other limiting factors e.g. light intensity etc affecting the rate of photosynthesis
Does the rate of photosynthesis affect the rate of aerobic respiration?
Hey guys,

Does the rate of photosynthesis affect the rate of aerobic respiration?
Thanks!
I suppose it could affect it if there was very little glucose (produced by photosynthesis) present to act as an input for aerobic respiration. It wouldn't happen naturally, but I suppose you could set up the conditions so that a slow rate of photosynthesis meant few inputs available for aerobic respiration (e.g. closed system with all oxygen coming from photosynthesis).
If photosynthesis occurs in a solution, why will the solution become alkaline?
If photosynthesis occurs in a solution, the solution will become alkaline. Why is this the case?
Well assuming the rate of photosynthesis exceeds the rate of respiration, therefore more CO2 is being consumed and O2 produced. Therefore there is less CO2 in the solution (converted into organic carbon in the form of glucose), therefore there is less carbonic acid (which forms when CO2 dissolves in water) and therefore the solution will become more alkaline.
This is a really excellent answer, nailed it.

Just want to highlight what you said about the rate of photosynthesis being higher. This is often not the case. In many the solution becomes more acidic! There's actually an experiment a lot of students do using phenol red indicator where this problem pops up.
Do I need to know that the light-independent phase produces G3P?
4) For the context of VCE, do I need to know about the light-independent phase producing G3P?
4) Nope
What’s the best answer when asked about the location of the light dependant reaction?
5. When talking about the location of the light dependent reaction, is it best to say on the grana/granum, or on thylakoid membrane or thylakoid disks or in the thylakoids?
5. VCAA has said grana before so I would go with that (2012 exam 1 Q8)
« Last Edit: November 27, 2018, 02:17:44 pm by PhoenixxFire »
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Re: Biology Q&A archive/Bio FAQ
« Reply #6 on: April 09, 2018, 09:37:48 pm »
+20
U3 AOS2 Cellular signals
Relevant study design dot points
• the sources and mode of transmission of various signalling molecules to their target cell, including plant and animal hormones, neurotransmitters, cytokines and pheromones

• the stimulus-response model when applied to the cell in terms of signal transduction as a three-step process involving reception, transduction and cellular response

• difference in signal transduction for hydrophilic and hydrophobic signals in terms of the position of receptors (on the membrane and in the cytosol) and initiation of transduction (details of specific chemicals, names of second messengers, G protein pathways, reaction mechanisms or cascade reactions are not required)

• apoptosis as a natural, regulatory process of programmed cell death, initiated after a cell receives a signal from inside (mitochondrial pathway) or from outside (death receptor pathway) the cell resulting in the removal of cells that are no longer needed or that may be a threat to an organism, mediated by enzymes (caspases) that cleave specific proteins in the cytoplasm or nucleus (details of specific cytoplasmic or nuclear proteins are not required)

• malfunctions in apoptosis that result in deviant cell behaviour leading to diseases including cancer.

Difference between necrosis and apoptosis?
Describe one difference between apoptosis and necrosis

Thanks :)
Necrosis involves cellular swelling, apoptosis involves shrinkage.

Cellular contents leak out into the extracellular space during necrosis, in apoptosis organelles/contents are released in apoptotic bodies

Necrosis is usually followed by an inflammatory response, apoptosis is not
What happens during apoptosis?
Enzymes, called caspases, are activated inside the cell which break down organelles including the cytoskeleton. In doing so, blebs form on the cell membrane as the cell's structure essentially collapses. The cell is then fragmented into apoptotic bodies which are then phagocytosed by phagocytes. The phagocytes contain lysosomes (organelles) which then break down the biomacromolecules into simpler molecules.
Where does the extrinsic signal come from in apoptosis?
5. Regarding apoptosis: where does the extrinsic signal come from?

Thank-you in advance!
5. Any number of places. Viruses. Damaged cells. Immune cells. It's just a signalling molecule, much like a hormone actually.
What are some things that trigger intrinsic and extrinsic apoptosis?
What are some reasons for a cell to induce apoptosis intrinsically?

What about extrinsically?
Intrinsic:
- DNA Damage (i.e UV light)
- Mitochondrial damage
- Lacks of growth factors
- ER stress
Extrinsic:
- Cell is no longer needed (i.e.certain immune cells after immune response)
- Cell is worn out or damaged (i.e. cells lining intestine)
- Cell is cancerous (i.e. unable to initiate intrinsic pathway)
Why aren’t interleukins hormones?
Why aren't interleukins hormones?
Interleukins are a type of cytokine. Cytokines differ from hormones in that cytokines are secreted by a wide range of cellular origins, while true hormones are only secreted from specific glands. Truth be told though, the distinction is often tough to make as there is a strong overlap between the definitions of hormones and cytokines in relation to immune function.
How do hormones cause a response?
How do hormones initiate the expression of genes?
Well particular hormones bind to intracellular receptors and initiate signal transduction (series of events/reactions that are dependent on each other) for a specific secretion or something of its kind (really depends on the hormone). This then leads to changes in gene expression as the hormone is solely functioning to stimulate specific cells or tissue/action.
Possible triggers of apoptosis
List three possible death signals a cell might receive to initiate apoptosis

Thanks  :D
If the cells are no longer needed,
if they are malfunctioning/ not working properly anymore,
if there are too many of the cells in the body. Think I'm missing one
How does apoptosis involve signal transduction?
How does apoptosis involve signal transduction? Is just that the cell gives the signal for the cell to be destroyed and that there is a cascade of events that follow this? (caspase enzymes are activated, DNA in the nucleus and organelles (mitochondria) are digested, the cell shrinks, blebs form on the cell membrane, phagocytes engulf the cell remnants etc). Would the response be that the cell is destroyed?
Yeah, the eventual response is cell death
Are all hormones proteins?
Are all hormones made of proteins?
No. Some are steroid based: corticosteroids for example.
Some are amino acids: thyroxine for example.
How do peptide hormones cause changes in cytoplasmic function/gene expression?
I understand how for steroid hormones they eventually attach to receptors to hormone- receptor complexes, and then this attached to gene to create mRNA for protein. But for peptide hormones how does it eventually cause changes in cytoplasmic function/ gene transcription, I understand that the hormone attaches to receptor on membrane which amplifies it but then I'm sorta confused after here
Signal molecules inside the cell are activated when the peptide hormone finds its receptor and in turn, activate proteins causing the result.
During autocrine signalling, does the signalling molecule leave the cell?
During autocrine signalling, does the cell secrete the hormone out of the cell, so it can then bind to the membrane receptor? Or does the hormone remain within the cell after production and bind to the intracellular receptor?

thanks x
With autocrine signalling, the cell first secretes (releases) the hormone, which then binds to receptors on that same cell.
What do autocrine/paracrine/endocrine mean?
Do the terms autocrine, paracrine and endocrine refer to the secreting cell or the hormone itself? Bit confused as some texts have mentioned 'endocrine cells' while i have also heard that these terms are a way of grouping hormones

thanks x
Autocrine signalling involves a cell secreting a hormone which then binds to on that same cell. Endocrine signalling occurs in the endocrine system where hormones are sent to cells all over the body through the bloodstream. Paracrine signalling involves sending signalling molecules to cells close by.
How do lipophilic/hydrophilic signalling molecules cause cellular responses?
Could someone explain the complete process of how a lipophilic hormone (steroid) enters a cell and thus signals the cell to carry out a response?

Conversely could someone also explain in contrast how a Hyrdophillic hormone (amino acid/peptide) accomplishes the same thing?

Much appreciated.
You don't really need to know these things exactly, but the basic mechanisms.

Lipophillic

Makes its way through the membrane and into the cell where it associates with a chaperone. This chaperone brings it into the nucleus, where it acts in a biochemical pathway that up regulates or down regulates transcription. In general, lipophillic hormones act as transcription factors.

Hydrophillic

Binds to a receptor on the membrane. These can be a number of different types.
If the receptor is attached to a protein channel, this can cause an influx or outflux of ions. Neurotransmitters are an example of this.
The receptor can also be a G-protein, which undergoes a conformational change and interacts with a secondary messenger that amplifies the signal in the cell. Essentially, that one binding causes the transmembrane protein to stimulate heaps of proteins in the cell so the biochemical effect of the signalling is amplified. That's the signal cascade.




Those are fairly basic concepts, but that should be well more than enough.
What is the difference between a signal transduction and a signal cascade?
Are there any differences between signal transduction and signal cascades???
I think signal cascades specifically refers to the cascade of events that is generated within the cell after signal transduction has been initiated (by the binding of a signalling molecule to its receptor)
What are the difference between animal and plant hormones?
What are the differences between animal and plant hormones? :/
Animal hormones act much more rapidly than plant hormones.
Animal hormones usually travel through the bloodstream whereas plant hormones travel through the phloem or xylem or even in the air (like ethylene, since it's a gas). 
Animal hormones aren't necessarily produced in response to environmental factors, whereas plant hormones are always (or almost always) produced in response to some environmental factor.
Plants don't secrete hormones from glands, whereas most animal hormones are secreted by ductless glands.
Explain what happens in signal transduction
Explain what happens in signal transduction
Thanks ;D
Signal transduction is the conversion of an external stimulus into one or more internal events through the binding of a hormone/signalling molecule to a specific receptor which triggers a cascade of events in the target cell (like activation of G-proteins and second messenger molecules that amplify the signal) which results in an amplified cellular response.
Are hormones excreted or secreted? What’s the difference?
Are hormones excreted or secreted? What is the difference between these two terms?
Thanks  ;D
Hormones are secreted through the blood.
Excretion refers to the removal of waste products eg faeces.
How do nerve impulses work?
Hi everyone,
I have a question about transmission of nerve impulses. I know that when a signal is transmitted along the axon of a neuron it is a electrical signal, but when it reaches the synapse does the neurotransmitter convert the electrical signal to a chemical signal so it can cross the synapse to the receptors on the dendrite of the next neuron?
Basically, when it reaches the synapse, it triggers the release of neurotransmitters (protein based) by exocytosis.The neurotransmitters cross the synapses and bind to receptors on the next neuron.
Neurotransmitters are chemical molecules that are released by exocytosis at the axon terminals and travel across the synapse to the dendrites of the next neuron.
Where do neurotransmitters bind?
How do neurotransmitters carry out their function?

Since they're protein based, do they attach to membrane receptors and initiate signal transduction?
Yep! Since the neurotransmitters are protein-based (water-soluble) they bind to specific membrane-bound receptors on the surface of the postsynaptic membrane. Neutrotransmitters are signalling molecules, so once they bind to the receptors, they trigger a cascade of events inside the cell (signal transduction like you said) which results in an amplified cellular response. The responses are varied; but generally neurotransmitters would trigger another action potential in the following neuron.
What’s the difference between signalling molecules and signal transduction?
Hi,
Could someone explain me the differences between signalling molecules and signal transduction?
These two ideas are really confusing me.

Thanks :)
Signalling molecules initiate a cellular response. Examples include hormones and neurotransmitters. Signal transduction, however, is the process by which the signalling molecules instigate the response-the cascade of enzymes that bring about a cellular response.   

So, to give an analogy, signalling molecules are like teachers giving students (or cells) a bunch of practice exams (instructions). If students complete the exams, then signal transduction has occurred and they'll score well (response). If not, then a response will not happen (receptor doesn't bind to signalling molecule) and students will therefore fail.

Okay, so my analogy was terrible ahaha but I hope that it clarifies things a little :')
What is signal transduction/amplification?
Would anyone be able to explain signal transduction/amplification?
In the context of VCE Biology, this is pretty much all you need to know for Signal Transduction.
Signal Transduction: Signal transduction refers to the series of events that occur after the receipt of a specific signal which is understood by a cell to produce a response.
(Often causes signal amplification as well. For hormones, the signal is either the lipid or protein hormone. Events are different based on these 2 types.)

3 Stages of Signal transduction:
Reception – the binding of the signal molecule (e.g. a hormone) to its specific cell receptor.
Transduction – the second messenger is formed in or released into the cytosol (the second messenger amplifies the stimulus and initiates the cell’s response).
Induction – activation of the cellular process.

EXAMPLES of Signal Transduction
• Lipophobic Hormones (peptides/amino acids)
1. Hydrophilic hormones – peptides or amino acids – travel in the blood and come to cell
2. Hormone must bind to G-protein embedded and traversing the phospholipid bilayer
3. This signals secondary messenger molecules to be released in cell as a result which causes signal amplification
4. These secondary molecules bind to cytoplasmic receptors initiating responses. The multiple secondary molecules allows different outcomes to come out of one signal

• Lipophilic Hormones (steroids) enter cell
1. Carrier molecule (protein which is hydrophilic) attached to the lipophilic steroid hormone carries the hormone through the aqueous blood to target cell.
2. Steroid hormone breaks off from carrier molecule, and diffuses directly through phospholipid bilayer into cell
3. The Steroid binds to another protein carrier molecule to travel through aqueous internal cellular environment
4. The Steroid travels to nucleus to stimulate or supress gene expression
Why is the endocrine system slower than the nervous system?
1). Why exactly is the endocrine system slower than the nervous system?
1. Nervous system is electrical (and chemical) whereas endocrine system is only chemical. The former involves neurotransmitters which travel between neurons over exceedingly small distances (think about synaptic gap) to reach their target cell whereas the latter involves hormones generally released into the bloodstream, and hence their target cells would be much further away. Also, nervous signals are more directed than hormones, which are carried by the general flow of blood.
Where does a steroid hormone bind to an intracellular receptor?
3). With steroid hormones, when the signal is received by an intracellular receptor molecule, what happens then? Some books say the complex moves into the nucleus, and others say that the complex forms inside the nucleus. Which one is it, or is it both?
3. Either. A steroid-receptor complex may form in the cytoplasm and then move into the nucleus or it may form in the nucleus.
Define signal transduction and outline the role of secondary messenger molecules
Hey guys! Can someone please answer these for me.

Define signal transduction.

Outline the role of secondary messenger molecules.

Thanks.  :)
Signal transduction is the series of biochemical reactions that occur once the hormone-receptor complex has been formed, and the signal has been received by the target cell.

When protein-based hormones (hydrophillic) bind to their receptor proteins on the outer surface of the cell membrane, they stimulate the enzyme on the inner surface of the membrane which then activate a secondary messenger molecule, which will then endure signal transduction (activate other enzymes for the cellular response).

I just recently covered this topic, so my help might be rusty :3, hope it helped!
Just remember to add that signal transduction leads to a cellular response!

Here are 3 points which summarise it:
1. Reception (the binding of the signalling molecule to its specific receptor)
2. Transduction (cascade of intracellular events which amplifies the original signal)
3. Response (leads to a cellular response).
What are the steps in the pathway of hydrophobic and hydrophilic hormones?
Hey can someone list the steps in the pathway of a lipid soluble hormone and hydrophilic hormone. Thanks!
Haven't read earlier responses in the thread, so I'm hoping this is what you want :)

Lipid soluble:
 - hormone diffuses through plasma membrane
 - binds with receptor in the cytosol
 - this directly interacts with the DNA, activating or suppressing a particular gene (in theory; I imagine in practice there are heaps of other molecules involved - I should research it :) )

Protein-based/hydrophilic:
 - hormone binds to plasma membrane receptor
 - this activates second messengers (e.g. G proteins, cAMP)
 - they then trigger a cascade of intracellular responses
How would you describe signal cascade?
How would you define the cascade effect in signal transduction?

Thanks
1. The significance of a cascade effect is that a single signalling molecule can exert a profound effect within a cell through the activation of a multitude of relay molecules. A single molecule can activate thousands upon thousands of other molecules within the cell, which then gives rise to a cellular response. You wouldn't need to define the 'cascade effect'; however, it's essentially the activation of relay molecules which subsequently initiates a chain reaction of more reactions.
Are hormones released into the extracellular fluid or the bloodstream? Is there a difference?
3. Can I say that hormones are released into extracellular fluid instead of the bloodstream? (Is there a difference?)
3. Absolutely not. Extracellular fluid is the fluid in which all tissues are bathed, whereas blood is fluid contained within the lumina (sing. lumen, just means a hollow tube) of blood vessels. Hormones are exclusively released into blood vessels and not extracellular fluid (technically hormones can be released into both, but they're not acting as a hormone if they're in the tissue, they're acting as a paracrine in that context—basically, paracrines and hormones can be the same molecule, just in different places).
Does signal transduction happen with lipid based hormones?
4. Does signal transduction happen with lipid-based hormones? I'm pretty sure it does but could someone just briefly explain the "cascade of events" that occurs?
4. It does. Lipid hormone comes in, binds its receptor and the receptor moves to the nucleus where it helps to transcribe genes. Post-VCE a lot more information is added to this, but you'll just have to accept that this is signal transduction even if it doesn't have the stages you're used to.
What is a signal cascade?
Hey guys,

Could someone please explain the term 'cascade' to me in terms of signal transduction of polar/non-polar signalling molecules, and where does it fit in each event.

Thanks in advance
A signal cascade is the sequence of biochemical reactions in which each reaction causes the next reaction to be possible. It's like a sequence of dominoes tipping each other over. In the transduction of polar ligands, the ligand (usually a hormone I think?) is unable to diffuse across the phospholipid bilayer so it binds to a membrane receptor. The receptor's shape (configuration) then changes - which in turn changes the shape of - and hence activates - a second messenger in the cell's cytosol. This activated second messenger then activates another second messenger which activates another second messenger which ... .   this is what we refer to as a signal transduction cascade. For a non-polar hormone, it diffuses across the phospholipid bilayer and binds to an intracellular receptor - forming a hormone-receptor complex. This complex may then act as a transcription factor - controlling the expression of particular genes. To my knowledge, no cascade occurs in this scenario.

That's only my understanding of it though, and I'd really appreciate if someone could read over it and confirm whether what I'm saying is actually correct!
Couldn't have explained it any better. That's pretty much exactly what happens.
What’s the difference between exocytosis and secretion?
Hey all, what's the difference between exocytosis and secretion?
Hello,
Secretion refers to ANYTHING that's discharged from the body of something (the body of a cell, organ, Pauline Hanson), for a particular function (including excretion, which is a type of secretion)
Exocytosis is more specific and it refers to bulk transport out of the cell via secretory vesicle. (note that exocytosis is a type of secretion).
How do I tell which molecule is the effector?
Just with signal transduction, is the effector the molecule that acts as a transcription factor and alters gene expression, or the protein that is produced as a result of it that has an effect on the cell? Thanks in advance!!
It would depend on the context of the question. If you start with a signalling molecule then the response would be a protein being produced which would make the transcription factor the effector because it carries out the response.

However if you start with the transcription factor being a stimulus for a response eg. lowering blood glucose levels then Insulin (the protein produced) is the effector because it carries out the response.

So it really depends on what your initial stimulus and your response are. Was it a particular question you were having trouble with or just a general query?
Why do hydrophilic hormones last longer than hydrophobic hormones?
Why do hydrophilic hormones last for a shorter time than hydrophobic hormones? They both lead to molecules directly activating or suppressing genes so why is this the case?
You wouldn’t need to know the answer to this question for VCE biology.

Peptide hormones have really short actions. Their influence is fleeting and they are rapidly degraded. Lipid hormones, however, remain active for a long period of time.

The reason for the difference has nothing to do with the molecules, but is actually all to do with the way cells deal with these hormones. Without going anywhere near the details, peptide hormones break down more quickly because that’s what cells do to them. Conversely, lipids stick around because that’s what cells do. These basically have to do with how long the hormone can stay bound to its receptor (which depends on the design of the receptor) and also whether there are many enzymes around to break them down.
What do we need to know about neurotransmitters?
can someone explain the detail we are required to know regarding neurotransmitters?

thanks

Know that an action potential (electrical impulse) causes them to be released from a pre synaptic neuron. They then diffuse across the synapse and bind to a ligand gated channel protein on the post synaptic neuron, which opens, allowing ions to enter, triggering an action potential in the post synaptic neuron.


What do intercellular/intracellular/extracellular mean?
Hey everyone,

can someone please explain to me the difference between intercellular, intracellular and extracellular

thanks

Intracellular: Inside the cell

Intercellular and extracellular can be used to mean the same thing but are slightly different.

Intercellular: Between cells.

Extracellular: Outside of cells (but still in the body).

Extracellular is normally used for things that have access to general body fluid, whereas intercellular is limited to a few specific cells. e.g. interneurons are intercellular messaging molecules whereas hormones are extracellular messaging molecules. Extracellular and intracellular are the terms you will use the most - intercellular is normally only used when talking about signalling.

Why does a hydrophilic molecule binding cause an intracellular reaction?
When a hydrophilic signalling molecule binds to a receptor on a cell, why does this cause the intracellular part of the receptor to change shape and activate molecules (e.g. second messengers, G proteins) inside the cell? Thanks :D
Very interesting question!

The "why" questions are often quite ambiguous pertaining to the amount of depth expected, though what I can intimate is that hydrophilic signalling molecules each contain various regions of charge, polarity or non-polarity etc. and it is these factors that - upon binding to the receptor - interact with accompanying charges (etc) at the site of ligation and ultimately cause a change in shape of the receptor (this is analogous to the method by which a protein confronts a change in shape during denaturation consequentially to encountering specific environmental factors). This change in shape, furthermore, alters the interactions between this receptor and substances within cells, thence triggering the characteristic signal transduction cascade.
What is the mode of transmission of neurohormones?
I swear I'm posting on here a lot but lowkey stressing about bio because school is about to start! (yaaaayyyyy)

What is the mode of transmission of neurohormones? (i.e. are they autocrine, paracrine or endocrine?) I'm fairly certain that they travel through the bloodstream so they probably are endocrine but just wanted to get your opinions, thx :p
Hey peachxmh,

All good - I'm pretty sure we're all feeling it haha :,)

Yep! The mode of transmission for neurohormones (in general) is typically endocrine as they travel in circulation.

Ah, the difference between neurohormones and neurotransmitters is that neurohormones are a wide range of things; they can act as neurotransmitters, but can also be secreted into the bloodstream and carried along to be received further away. Neurotransmitters are simply used to bridge the short gap between two nerve cells (synaptic gap), and the name 'neurotransmitter' is just specifying what kind of neurohormone we're talking about.
Hope this helps!
~poet xx
What do we need to know about apoptosis?
Hello again :) I did a quick search of the forum but couldn't find an answer to my question so I figured I'd ask it in case anyone else wanted to know as well. To what extent are we required to know about apoptosis? Do we need to know about Bcl-2 or Apaf-1? Many thanks!
You don't need to know them
You just need to know the general process i.e. Extracellular signal or mitochondrial signal - Caspases cleave the cytoskeleton - cell collapses and forms apoptotic bodies (also called blebs) - the apoptotic bodies are engulfed by phagocytes and the contents recycled.
Do we need to know about negative feedback or stimulus response?
do we still need to know about the negative feedback model and stimulus response model in year 12 bio
You don't need to know much about the negative feedback model, but the study design now puts a lot more emphasis on the stimulus response model
What is cytokines mode of transmission?
I read somewhere that cytokines mode of transmission is autocrine, paracrine and endocrine.

is this right?

cheers
Yes, that it correct!
thanks.

I understand how it can be endocrine, since it can enter general circulation, but can you explain how it is paracrine or autocrine

cheers
So an example of this is the cytokines released by T helper cells. When a B cell that has bound its antigen finds a T helper cell that has been activated by an APC the Th cell will release cytokines. There cytokines cause both the Th cell and the B cell to divide and differentiate. The cytokines are released from the Th cell, and are acting on the Th cell so they are autocrine. They are also acting on a nearby cell (the B cell) so they are paracrine.
What level of detail do we need to know about plant hormones?
Hey guys,

Do we need to know about specific plant hormones such as auxins? What level of detail should we know?
Thanks!
For plant hormones, you should have a general idea of each one does - you don't need to know them in a lot of depth.
What is the transduction step for hydrophobic signalling molecules?
How would one describe the "transduction" step for hydrophobic signalling molecules, because for hydrophilic it is synthesis of second messengers? If someone was to describe signal transduction in general, wouldn't there be a different transduction process?
The transduction step for hydrophobic signalling involves the movement of the signal-receptor complex to the nucleus and subsequent steps required for a response to take place (i.e. binding to DNA or activating another transcription factor, transcription, translation etc.)

EDIT: I didn't answer your second question, which I just realised. The definition for signal transduction (stripped right from VCAA): "Signal transduction refers to the series of events that occur after the receipt of a specific signal and which result in a response". This is a highly broad definition that effectively encompasses both hydrophobic and hydrophilic signalling.
What's the difference between protein-based and peptide-based hormones?
1. What's the difference between protein-based and peptide-based hormones?
1. Protein based hormones have longer amino acid chains than peptide-based hormones. You don't need to distinguish between them for VCE though, you just need to know that some hormones are amino-acid based (amine, peptide, protein) and some are steroid based.
What does the "recycling of cell debris" stage of apoptosis comprise of?
2. What does the "recycling of cell debris" stage of apoptosis comprise of?
2. Not really sure on this. I think it just means that after blebs have been phagocytosed the individual components are reused in the body. Not sure whether they would be broken down into base components or entire organelles reused or what though.
What is the final stage of apoptosis?
3. What is the final stage of apoptosis? Signal for macrophages? Cell fragments into apoptotic bodies?
3.
According to VCAA 2016
Quote from: Q3.c.
As a wound heals, cells that are no longer needed for the healing process are removed by apoptosis.
Apoptosis is stimulated by external cell signalling from cells such as cytotoxic T cells (Tc).
    Outline the main stages in cell apoptosis once stimulated by the Tc cells.

Quote from: suggested solutions
Possible answers included:
• enzymes; for example, caspases are activated within the cell
• digestion of cell contents
• cell shrinkage
• cell blebbing
• cell breaks up
• cell signals macrophages.
Phagocytosis of cell debris was not accepted.
So I'd take this to mean that VCAA believes 'signal for macrophages' is the last step.
What does signal transduction refer to?
Does signal transduction refer to the stage in between reception and response or does it refer to the entire process? If not, what is the entire process called (is it stimulus-response model)?
Both. The process is called signal transduction and the three steps are
1. reception
2. transduction
3. response
just to make it even harder for us haha
Do autocrine signalling molecules only effect the cell that produces them?
Do autocrine hormones only affect the cell the cell that secretes them or the same type of cell
3.
Only the cell releasing them. It's not only hormones by the way - cytokines can also have autocrine signalling. Also something can be both autocrine and paracrine so it doesn't necessarily just affect it, but only the part where it effects itself is called autocrine.
What are the differences in transduction for hydrophilic and hydrophobic signalling molecules?
Also, what are the differences in transduction for hydrophillic and hydrophobic signalling molecules !!!! Thankyou!!
Hydrophilic signalling molecules cannot pass through the plasma membrane, so they bind to a membrane bound receptor, which causes internal changes that leads to a second messenger molecule inside the cell (there are some pretty cool videos of this on youtube which might help if that’s confusing). Hydrophobic signalling molecules can pass through the plasma membrane, so they enter the cell and bind to an intracellular receptor in the cytosol.
How much do we need to know about caspases?
1) Do we need to know the different types of caspases?
1) You don't need to know the different sorts of caspases, just know that caspases exist.
How does the intrinsic pathway of apoptosis work?
Could someone please explain how the intrinsic apoptosis pathway works?
The intrinsic pathway is mediated by the mitochondria. When the cell recognizes stress, irreparable damage, aberrant activity (or a bunch of other things), the mitochondria will release cytochrome C. This will activate caspases which (in a signal cascade) activate other caspases as well as cleave cellular elements like the cytoskeleton. This causes cell breakdown, blebbing and the eventual formation of apoptotic bodies.
« Last Edit: November 27, 2018, 02:18:16 pm by PhoenixxFire »
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Re: Biology Q&A archive/Bio FAQ
« Reply #7 on: April 09, 2018, 09:38:44 pm »
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U3 AOS 2 Responding to antigens part 1
Relevant study design dot points
• an antigen as a unique molecule or part of a molecule that initiates an immune response including the distinction between non-self antigens, self-antigens and allergens

• invading cellular and non-cellular pathogens as a source of non-self antigens, and preventative strategies including physical, chemical and microbiological barriers in animals and plants that keep them out

• the characteristics and roles of components (macrophages, neutrophils, mast cells, dendritic cells, complement proteins) of the innate (non-specific) immune response to an antigen including the steps in the inflammatory response

• the role of the lymphatic system in the immune response including the role of secondary lymphoid tissue (with reference to lymph nodes) as the site of antigen recognition by lymphocytes, and as a transport system for antigen presenting cells including dendritic cells

• the characteristics and roles of components of the adaptive (specific) immune response including the actions of B lymphocytes and their antibodies (including antibody structure) in humoral immunity, and the actions of T helper and T cytotoxic cells in cell-mediated immunity.

Do some antibodies remain in the body after an immune response?
I just want to clarify that after an immune response, there will still be some antibodies circulating the system despite most of it being broken down? Or are all antibodies produced by plasma cells at the time of infection broken down and just the memory cells remain?
Yeah, some antibodies specific to the antigen will remain in circulation after the infection is gone (with the concentration gradually reducing over time)
What is the difference between cytotoxic T cells and natural killer cells?
What is the difference between cytotoxic T-cell and natural killer cells?
Cytotoxic T-cells are part of the cell mediated specific immune response, whereas natural killer cells are part of the non-specific immune response; T-cells recognise antigens, whereas NK cells do not.
This is outside of the scope of the VCE course, but its some extra interesting info about it and you can find it in the Nature of Biology textbook if you use it. So basically, Natural Killer cells have two receptors, a killer activation receptor (KAR) and killer inhibitory receptor (KIR). KAR binds with surface proteins released by virally infected cells or cancerous cells in distress, while KIR binds to MHC Class I markers on the cell. If the KIR binds with a sufficient number of MHC Class I markers, then the order to kill is overridden. (We can get a lack of MHC Class I markers when viruses or cancer cells inhibit or destroy MHC Class I markers on the cell surface). Therefore, if the cell is lacking of MHC Class I markers, then the signal to kill won't be overridden and then the NK cell will secrete perforin damaging the plasma membrane leading to lysis. If the cell has sufficient MHC Class I markers, then I'm pretty sure that those cells are left for cytotoxic T cells.
What is the difference between lymphocytes and leukocytes?
Also what is the difference between lymphocytes and leucocytes?
I think leukocytes are the general term for cells of the immune system, whereas lymphocytes are those that are part of the specific immune system such as T and B lymphocytes.
Just to add to this, NK cells are also lymphocytes even though they're not a part of the adaptive immune response (they're innate and non-specific). Leukocyte is the scientific name for white blood cells.  :)
What is the role of cytokines in the immune response?
What is the role of cytokines in the immune response?
Cytokines: Proteins produced by all cells of immune system which act as intracellular messengers to convey signals within the immune system. Interleukin is a key example of a cytokine. IL-1 resets the hypothalamus (creates fever) and recruits T- Helper cells) while IL-2 activates B cells (which is the humoral response) and activates T-Cells (which is a cell-mediated response)
What are the functions of the five types of immunoglobins (antibodies)?
Does anyone have a list of definitions and functions for the 5 type of immunoglobulins?
-IgG
-IgA
-IgM
-IgE
-IgD

Thanks :)
-IgG - Has a life span of 21 days, mostly circulating antibodies and function in agglutination and complement activation.
-IgA - Has a life span of 6 days, found in external secretions, tears, saliva and milk. Functions as mucosal immunity.
-IgM - Has a life span of 10 days, produced early in infection response and function in agglutination and complement activation.
-IgE - Has a life span of 2 days, produced in allergic reactions and attaches to mast cells.
-IgD - Has a life span of 3 days, located on the surfaces of antibody-producing cells (B lymphocytes)  and are responsible for the development of antibody response.

The SD doesn't explicitly say to know these. However IgD and IgE are two I would make sure I knew. :)
Do all pathogens cause disease?
Do all pathogens cause disease? If not why? I was under the impression that an infectious disease is caused by a pathogen, but my text book tells me not all pathogens cause disease.
Firstly, a pathogen is a "disease-causing organism or agent". However, this does not necessarily mean that every pathogen brings about disease in a host; rather, they may have the potential to cause disease (pathogenicity), but the host's immune responses prevents it from doing so. Or sometimes, they only cause disease under certain conditions/circumstances (e.g. opportunistic pathogens).

This is because a disease is defined as that which harms the normal functioning of the body. So if an organism is not 'harming' the body, then it's not acting as a "disease-causing agent".

Edit: yes, an infectious disease is always caused by a pathogen, by not all pathogens get the chance to cause disease in a host organism.
What is the role of antibodies?
What is the role of antibodies? Do they bind with antigens to help facilitate phagocytosis by clumping them together or is there more to it?
More to it, but that's one thing they do. They can neutralise things that come in and they can also promote phagocytosis as you suggested. They're also pro-infammatory and can activate complement.
What is the purpose of MHC markers?
What is a perfect definition of an antigen?
What is a perfect definition of an antigen which would get full marks?
5. A foreign body that induces the production of antibodies. (antibody generating).
How do helper T cells activate B cells?
Anyone know how a helper T cell activates the other lymphocytes?  :-\
Most B cells require 2 signals to be activated and begin clonal proliferation and differentiation into plasma and memory cells:
1. B-cell receptor binds to specific antigen.
2. T helper cells (which have been activated by that specific antigen) then secrete cytokines/interleukins (messengers between immune system cells) which bind to and stimulate/activate the B cell.

So essentially, B cells can't multiply and become antibody-producing plasma cells just by running into the appropriate antigen; they NEED a T helper cell to send them cytokines.  You don't have to know more than this (e.g. what the specific cytokines are, or how it all works).
How do cells detect non-self material?
Hey guys,

 I was just wondering if someone could give me a summary of how cells detect foreign materials from self materials, which cells detect this and how cells detect viruses? Another thing I am not fully understanding is the MHC markers.

Thanks!

There are a number of ways that cells can recognise non-self. Certain cells of the immune system express receptors that can bind molecular markers that are relatively common in pathogens but never appear in humans. For instance, these receptors might bind double-stranded RNA, which occurs in some viruses but certainly not in human cells.

B-cells express receptors that are able to bind free antigens. These are molecules that are part of or produced by pathogens that float around in tissue. B-cells can bind a whole host of these molecules. They do not, however, typically express receptors to self molecules (how this happens is well beyond the course but basically any B-cells that express receptors to self antigens are deleted).

T-cells, on the other hand, express receptors that can bind antigens (i.e. molecules from pathogens) that are presented on MHC markers. MHC class I markers present antigens (they just hold them) that originate from inside the cell. Therefore, if a cell is infected by a virus, molecules from the virus are expressed on the surface of the cell. T-cells will recognise these molecules as foreign and will respond accordingly. MHC class II molecules are expressed on a limited number of cells. These molecules present antigens that have come from the environment. T-cells can bind antigens presented on these MHC molecules if they are non-self.

What’s the difference between antibodies, antigens, and MHC markers?
Hey everyone

I keep getting confused with antibodies, antigens and MHC markers. Can someone please distinguish them for me? I have not done immune system before so any help would be greatly appreciated. <3

Antigens: they are group of compounds, typically proteins which provoke/trigger an immune response, including the production of antibodies.
Antibodies: protein molecules designed to attach to only one specific type of antigen.
MHC Markers: In order to to distinguish non-self from self molecules, MHC markers are located on the surface of cell membranes.
Class 1 MHC Markers: located on the surface of all human cells with a nucleus (except RBCs). They display peptide fragments produced within the cell.
Class 2 MHC Markers: located on antigen-presenting WBCs. They present peptide fragments that they have engulfed via phagocytosis.

Physical and chemical plant defences?
what plant defences (both physical and chemical) are we required to know for the exam? If a question asked to list a few physical and chemical plant defences, what could you say?
*pulls out VCAA definitions and processes document*

(surprisingly, it's really handy for myself too :D) So these are answers from past questions they've asked:

Barriers in plants:
•   Waxy layers on outside surface
•   Intact or thick cuticle
•   Chemicals that repel potential pathogen vectors such as insects
(Not from the exam report but my own knowledge: another could be thorns and hairs to deter vectors, or excreting nasty chemicals that kill pathogens - no need to be specific)

And if infection does occur in plants:
•   Grow ‘gall’ tissue round area containing infective agent to prevent spread to other areas
•   Produce chemicals e.g. tannins
•   Produce ‘gum’ to seal off wounded area
•   Drop infected leaf to inhibit spread to other areas
What happens to a macrophage after it engulfs a foreign pathogen?
When a macrophage engulfs a foreign pathogen, it digests and degrades it. Antigenic fragments are then presented on the MHC II markers. What happens now? Where does this macrophage go, or what comes to it?
The activated macrophage will carry the antigen (on its MHC class II) to the lymph nodes, where T cells are accumulated, improving the chance of finding the matching helper T cell.
The macrophage then releases interleukin-1 to activate helper T cell.
Can the 2 variable regions on an antibody be different?
Can the two variable regions on an antibody be different?
Thanks  :)
the variable region has to be identical because it is specific for a particular antigen.
Why do phagocytes have a large number of ribosomes?
Why do phagocytes have a large number of ribosomes?
Help would be greatly appreciated.
Thanks in advance
Phagocytes need lots of ribosomes to manufacture digestive enzymes which fill the lysosomes to destroy any foreign material engulfed by the cell.
How are B cells activated?
Hey  :)

Could someone please explain to me how B Cells are activated? And the role of T Helper Cells in activating the B Cells, I'm confused  :'(
B-cells get activated when they bind to a specific antigen. It will then proliferate and differentiate into two different cells 1. Memory cells, basically the same as the parent cells(same antibody for the specific antigen) and plasma cells, these produce and secrete anti-bodies for the specific antigen.
T helper cells can only bind to antigens located on the MHC 2 protein in contrast to cytotoxic T cells. T helper cells activate B-cells by releasing cytokines to the B-cell that it is binded to. *Im sure these are correct, but if there is anything wrong, feel free to correct me*
Can APC’s only present antigens to Tc cells?
2) Can APC's present antigens to cytotoxic t cells as well or just helper t cells?
2.APCs can present to both. Antigens on MHC2 markers will be presented to T helper cells and antigens on MHC 1 markers will be presented to cytotoxic T cells.
Just to clarify: They can only present antigens whilst performing their function to a Th cell. However, they can also present fragments of their own polypeptides to Tc cells, as all cells can do (except red blood cells).
How can we identify a pathogen?
Also, how do we identify pathogens?
There are actually a few ways to identify a pathogen (bacteria or virus, in this case)
Bacteria:
- agglutination test (with specific antibodies)
- precipitation test (to see if a bacterial colony precipitates in the blood of an infected person)
- Western blot test (used to separate and identify proteins specific to a bacteria)
- ELISA (enzyme-linked immunosorbent assay, which is used to detect and count substances such as antibodies, hormones, enzymes and antigens, which indicates the type of bacteria we might be looking for)
Virus (these things are smaller, so we have to use more precise techniques to kinda sort them out)
- ELISA
- X-ray crystallography (which is used to determine the atomic and molecular structure of crystals, can be used to identify viruses of specific shapes and sizes)
- Electron microscope (these things let you see really small things so you can see viruses with this)
How are cytotoxic T cells activated?
Hi all,
Can somebody please explain how Tc cells are activated? Do they require Helper T cells at all?
Thanks in advance :)
My understanding is that Helper T cells bind to infected cells and release cytokines which attract Tc cells. Then the Tc cells bind to the virus-infected cell and secrete perforins, inducing lysis.
Hi!  :D

Cytotoxic T cells recognise and bind to the antigens presented on the MHC-I markers on cells that are cancerous or virally infected and the binding of the Tc receptors causes a signal transduction in the T cell, resulting in it proliferating and differentiating into active Tc cells and memory T cells. And I'm pretty sure that the cytokines that the helper T cell produces helps the Tc cell to proliferate and differentiate.

The Tc cell then releases perforin to destroy the plasma membrane of the infected cell to kill it or may kill it by binding to the infected cell's death receptor.

*someone please correct me if neccessary  :)
Both answers above are pretty close.

Cytotoxic T-cells do bind to MHC class I molecules on cells that are infected with an intracellular infection. Cytokines from multiple sources help to stimulate the T-cells, as do signals directly from T-helper cells.
How are B and T cells activated?
Can someone please tell me how B and T cells are activated, the answers my teacher and the exams give are so ambiguous  :'(
B cells are activated by free antigens (ie parts that have broken off) binding to them. T helper cells are activated by an antigen that they can bind to being presented to them on MHC 2 markers by an Antigen Presenting Cell (APC) ie. dendritic cells and macrophages.The activated B cells and T helper cells then find each other and if they have the same specificity (have bound the same antigen) the T helper cell will release cytokines (a type of signalling molecule) that further stimulate both of them to divide and differentiate. Cytotoxic T cells are activated when they can bind to a peptide fragment presented on an mhc 1 molecule. They can also be further stimulated by the cytokines but do not need to interact with t helper cells.
What causes histamine to be released?
1. What are the causes of the release of histamine?
1. There are many causes: Damage to the surrounding tissue, cross linking of bound antibodies (an allergic response), it can also be released by some medicine (including morphine and some antibiotics - but we don't need to know this)
Overview of intracellular (cell-mediated) immunity
General process always occurring in our bodies:
-B cells mature in the bone marrow. Here they are tested for self-reactivity, if they can bind to a self antigen they are normally destroyed (except for malfunctions ie autoimmune diseases.)
-Both Tc cells and Th cells mature in the thymus gland. Here they are also tested for self reactivity.

Throughout the body there are always B cells, Th cells, and Tc cells with a randomly generated antigen specificity.
B cells are found in lymph nodes (and throughout the lymph system)
Th cells are found in lymph nodes
Tc cells are found throughout the body tissues.

Normally:
B cells and Th cells just hang about waiting for their antigen to bind/be presented to them.
Tc cells travel throughout the body attempting to bind to peptide fragments presented on MHC1 markers.

If an intracellular pathogen (ie virus) enters the body, parts of it will inevitably end up in the blood and lymph. Some of it will enter cells and cause the creation of non-self peptide fragments which will be presented on MHC 1 markers at some point. The following will happen simultaneously.

Humoral Immunity will be activated:
-A naive B cell will bind to a free antigen (ie. not presented by an APC).
-A Th cell will be presented with its antigen on a MHC2 molecule by an APC.
-The 'selected' B cell and Th cell will then find each other and if they have bound the same antigen, the Th cell will release cytokines (the same cytokines that affect cell mediated immunity - see below.)
-These cytokines cause the B cell to divide (proliferate) and differentiate into B memory cells and B plasma cells.
-These cytokines also cause the Th cell to divide (proliferate) and differentiate into Th memory cells and Th active cells.
-The memory cells remain in the body to fight subsequent infection by a pathogen with the same antigen specificity and the B plasma and Th active cells fight off the current infection.

As the pathogen (virus) is intracellular, cell mediated immunity is also activated.
-Naive Tc cells are always travelling throughout the body, attempting to bind to peptide fragments presented on MHC1 markers.
-When they find one that they can bind to, the Tc cell is 'selected'.
-The Tc cell will release granzymes (including perforin) which causes the cell to undergo apoptosis.
-The Tc cell continues to travel throughout the body and kill cells presenting the same peptide but it will not divide and differentiate until cytokines are present.
-When cytokines have been released from Th cells (this could happen before or after the Tc cell is selected) the Tc cell will divide (proliferate) and differentiate into Tc memory cells and Tc active cells.
-The Tc memory cells will remain in the body to fight off subsequent infection by the same pathogen.
-The active Tc cells will travel throughout the body, inducing apoptosis in cells presenting the same peptide fragment.
What is the role of cytokines in the immune response?
What is the role of cytokines in the immune response?
Cytokines: Proteins produced by all cells of immune system which act as intercellular messengers to convey signals within the immune system. Interleukin is a key example of a cytokine. IL-1 resets the hypothalamus (creates fever) and recruits T- Helper cells) while IL-2 activates B cells (which is the humoral response) and activates T-Cells (which is a cell-mediated response)
What are antigens?
Are antigens always referred to as foreign substances; don't all cells have antigens even self cells?
No, antigen means anything that generates an adaptive immune response.
Antigens are not always foreign but the ones your body actually mounts a full fledged immune response to are usually foreign.
antibody generating
Does tissue rejection involve natural killer or cytotoxic T cells?
When tissue rejection occurs, do only NK cells attack the 'non-self' tissue? Can it also be Cytotoxic T cells? Thanks.
CTL can definitely attack non-self tissues.  NK cells can't technically differentiate between self and non-self in a specific sense because they are innate cells.  CTL are the ones that will recognise specific non-self proteins on the surface of the cells.
Are needles vectors?
Also can vectors include needles?
Needles can't be vectors - vectors need to be living things that can carry an infectious organism from one host to another.  A needle is closer to a fomite.
What is Clonal Expansion?
Could someone explain the basics of Clonal Expansion? Everywhere I look is confusing and too complex haha
clonal expansion just refers to the differentiation of B cells which are part of the humoral response. B cells can produce 2 cells including B-plasma cells and B-memory cells.
Would you say T helper cells initiate clonal expansion?
Yes. They would have to initiate clonal expansion of certain B-cells/T-cells (that have a specific antibody-like receptor to the antigen)
Do antibodies in the body remain higher after a secondary immune response?
In the secondary antibody response why does the level of antibodies in the bodily fluids remain higher for a longer period of time than in the primary antibody response?
Well in Humoral immunity, T helper cells initiate the differentiation of B cells when exposed to a non self cell. The B cells become either memory or plasma cells, the memory cells remain in the body for a longer period of time, providing a rapid immune response (the secondary response). This is achieved by developing plasma cells much quicker than previously, destroying the pathogen before it can affect the host. Also known as the immunological memory.
What is the difference between MHC markers and antigens?
What is the difference between MHC markers and antigens?
MHC markers are proteins that are on a cell which indicates to the organism's immune system that it is a self cell. Examples of cells with MHC markers include macrophages, B cells and dendritic cells. An antigen are also proteins, an agent; pathogen, that 'binds' to an antibody, initiating a immune response.

However MHC markers, in the instance of an organ transplant can go under 'attack' as they are recognised as non-self cells as that organ does not possess the appropriate MHC markers.
What causes swelling and itchiness in the inflammatory response?
Does the swelling from inflammation result from leaky capillaries or vasodilation which brings more blood to the site?

Also, what causes the itchiness from inflammation?
Leaky capillaries causes an accumulation of fluid in the tissues, causing the swelling. This fluid carries phagocytes to the sites of infection.

Itchiness/pain is probably a result of increased pressure on surrounding nerves due to that swelling.
What is the difference between a leucocyte and a lymphocyte?
What's the difference between a leucocyte and a lymphocyte?
Leukocyte is a white blood cell
Lymphocyte is a group of white blood cells (T-cells and B-cells)
Function of MHC1/MHC2?
Hey guys, can somebody please help me out with MHC markers, I'm still quite confused about them! From what I understand:
MHC Class 1: Found on all nucleated cells
MHC Class 2: Found on B and T cells and macrophages
Could someone please help me with the function of each class and anything else we should know about them? thanks :)
MHC class I presents things that are inside the cell, whereas class II presents things that have been found in the environment. So if there's a virus in a cell, that'll pop up on class I and will "encourage" the immune system to kill it.
MHC 2 - Found on APC that present antigens to Helper T cells, which relay messages to either B or T cells with cytokines to begin proliferation
Please explain the differences between MHC1 and MHC2
can somebody please explain the process of macrophages and displaying MHC1 markers?
-Macrophage encounters a non-self antigen expressed on a pathogen/agent/substance, engulfing it. 
-The engulfed substance travels in a vesicle within the macrophage and fuses with a lysosome, where it is broken down into fragments.
-One of these peptide fragments then complexes with an MHC II and is expressed on the plasma membrane of the macrophage.
-Macrophages are APCs, therefore they possess MHC II molecules for the sole purpose of signalling the adaptive immune response upon foreign invasion.

Every nucleated cell (therefore not RBCs) expresses MHC I. Consequently, MHC I are 'self' detectors. As all MHC receptors have the capacity to express peptide fragments, infected cells will have foreign proteins complexed with their MHC I receptors. Normal cells will possess 'self' peptides complexed with their MHC I molecules. This establishes the differentiation between 'self' and 'non-self'

Therefore, MHC I does express 'self', HOWEVER upon infection (say by a virus) the molecules will express obscure peptide fragments which indicates to the immune system that the cell is not healthy. Then, NK cells (antigen non-specific) or Tc cells (antigen specific) will destroy the affected cells.

I hope that makes sense :)
Difference between primary and intermediate (secondary) host?
Can someone please distinguish between a primary host and an intermediate host? Cheers!
Primary host --> Host that the adult parasite lives in/on

Intermediate host --> Host that the larval parasite lives in/on
Primary host: site of sexual reproduction
Secondary host: site of asexual reproduction
Do plants have specific immunity?
Do plants have specific immunity? If yes, can someone please explain the concept? Thanks!
No. Plants only have physical and chemical barriers to stop pathogenic agents from entering the internal environment of the plant organism. This includes things like the formation of galls to trap and prevent the spread of a pathogen, etc. No specific attacks are made against specific strains of pathogens, and no memory is involved.
Does that mean plants die if a pathogen gets into their internal environment?
Thanks Yacoubb! So if a pathogen does manage to enter into the internal environment, does the plant have no other choice but to essentially die? Do plants possess anything similar to the mechanisms of a white blood cell?
There are different means by which the plant can try to protect itself. For instance, the formation of a gall. This gall is just a mass of tissue that forms around the site where the pathogen enters, which traps the pathogen, and prevents it from spreading to other parts of the plant.

However, its more than likely the plant will die if it is infected by a pathogen, because of its limited immunity to pathogenic agents.
What are the differences between basophils and mast cells?
What are the differences between basophils and mast cells, are they interchangeably used in inflammation, allergies
Relatively carry out similar functions; however differ in origins, sizes, shapes of nucleus, and their locations in the body. Are responsible for similar allergic reactions, and they both are made in the bone marrow, however, they are derived from different progenitors. As basophils mature in the bone marrow then travel throughout the blood stream, whereas mast cells leave the bone marrow in an immature state, and mature in body tissues.

In the case of inflammation, my thought is that they are interchangeable as both produce histamines. Not too sure about that one though!
(might want to check up on that)
If you're discussing inflammatory or allergic reactions, refer to mast cells, not basophils. Basophils are very unlikely to come up in the exam
How do mast cells help kill pathogens?
Is someone able to help me out with the inflammatory response?

I understand that mast cells release histamine which causes blood vessels to dilate, drawing more blood to the region and increasing heat, redness and swelling.

What I don't understand is how this actually kills the pathogen?

Thanks
It facilitates the process
Exactly what grannysmith said, it literally makes the blood vessels more permeable and hence the phagocytic cells are easily transported to the damaged tissue.
Local dilation of capillaries --> blood flow through area is more rapid (which may cause erythema) --> phagocytes can be transported to area more rapidly and destroy

Release of histamine increases permeability of local capillaries --> phagocytes more rapidly able to diffuse out into the interstitial spaces. Plasma also leaks excessively from the capillaries and accumulates in the interstitial spaces (plasma leaks more rapidly from capillaries than it can be returned to circulation via the lymph vessels), which causes swelling
Simple explanation of humoral and cell-mediated immune response
Can anyone give me a simple explanation of humoral and cell-mediated response?
Simple? I don't think thats possible haha!

Well Humoral and Cell-Mediated responses fall under the 3rd line of defence also known as the specific/adaptive immunity.

Humoral:
  • B-lymphocytes are the major cells involved.
- Produced in the Bone Marrow (thus the name B-lymphocytes)
  • Each B-Cell has its individual antibody/antigen complex
  • Production of antibodies
  • B-Cells differentiate (clonal expansion) into
- B-Plasma cells (effector cells): secrete antibodies
- B-memory cells: remain in the body so when the antigen is encountered again, a response can rapidly be reenacted.

Cell-Mediated:
  • Carried out by T-Cells
  • T-Cells made in the Bone Marrow however matured in the Thymus (hence its name  T-Cells)
  • T-Cells include; Helper T cells (Th), Cytotoxic T cells (Tc) and Suppressor T cells.
  • Helper T cells active cytotoxic cells and present antigens to immature B cells.
  • Cytotoxic cells detect/recognise cells with infection, are able to destroy these foreign cells with contact
  • Lastly Suppressor T cells, literally suppress the immune responses once the antigen has been removed
How do antibodies work?
Do antibodies, when they attach to antigens, inactivate the antigen themselves? Or do they act as a marker to attract other cells to engulf the antigen?
Antibodies; are proteins that bind and neutralise antigens. Are quite specific (like an enzyme-substrate complex).
Antibodies do not engulf the antigen. They bind to it and make it easier for phagocytes to find. They also make the antigen larger. This can stop them from working (e.g. They cause snake venom to agglutinate).
Do all Antigen presenting cells have MHC2?
Do all antigen-presenting cells have MHC class-2 markers?
Yes. Antigen-presenting cells such as macrophages, certain B cells and dendritic cells express MHC class II. The fragment of the antigen is bound there for the T cell to recognise.
What are granulated cells?
What are granulated cells and how does granulation assist in their functioning?
Granules are small packets of enzymes and other substance for example inflammatory chemicals like histamine. --> that are made up by Leucocytes that assist them in performing their function. For those white blood cells that are phagocytic (macrophages, etc) the enzymes in the granules (vesicles) will be released onto the eaten foreign material and break down its component pieces; hence bacteria is killed. The enzymes have to be kept in these designated vesicles because if they were free inside the white blood cell, they would destroy it from the inside.

Hope this helps :)
What is the cell mediated response? What do MHC markers do?
Can somebody please explain the cell mediated response?
also, where do MHC markers come into play
The cell mediated response is basically when the cytotoxic T-cells directly acts upon the virus/cancerous/fungi affected cells. For example, when a phagocyte (or other antigen presenting cells such as dendritic cells) engulf the pathogen (which could be a virus) it presents the non-self antigen fragments of the pathogen on its MHC marker on the surface of the cell membrane. The MHC marker in this case basically acts like a 'stage', kind of like a 'trophy holder' and stimulates the T-helper cell. The type of the marker would be class-2 since it is an antigen presenting cell and the stimulation of the T-helper cell would occur by interleukin-1 or you can just say cytokines and also matching receptors. The T-helper cell will then stimulate inactive T-lymphocytes to undergo clonal expansion and to differentiate into cytotoxic-T cells, T-supressor cells and T-memory cells.
The cytotoxic-T cells destroy virus-infected cells by releasing perforins (a kind of protein) which punches holes and lyses the membrane of the infected cell.

I hope this helps you somewhat and please, anyone correct me if I am incorrect!

(EDIT: beaten :P)
What’s the difference between mast cells and basophils?
Are Mast Cells and Basophils the same thing? Other than promoting an inflammatory response and blood flow through the secretion of histamines, do they have different distinct functions?

Quite confused tbh :/ Our teacher hinted to say Mast Cells instead... however is there a difference? Or is it just a different name?
They are different cells.  Basophils usually move through the circulation whereas mast cells are localised to the tissues.  They have similar functions and coordinate similar responses :)
Mast cells usually act earlier in the response (eg allergic response) because they're localised to the tissue.  They can recruit basophils to the site from the circulation.
What’s the difference between a parthenogenic organism and a parthenogenic agent?
What's the difference between a pathogenic organism and a pathogenic agent ??? Thanks ! :)
Organisms are living, agents are usually reserved for viruses, viroids, prions which are non-living
Why does first exposure to an allergen produce less severe symptoms?
Explain why first exposure to an allergen produces less severe symptoms than subsequent exposure
I know it has something to do with memory cells.
Thanks
2 main reasons are: B-memory cells have already been produced after fist encounter => response faster, more cross-linkages occur between the allergens and IgE antibodies bonded on mast cell, the release of histamine will also increase on second exposure.
What is the difference between a macrophage and a phagocyte?
What is the difference between a macrophage and a phagocyte?
A macrophage is a type of phagocyte. There are other types of phagocytes such as neutrophils and dendritic cells.
Similarities and difference between Natural Killer cells and cytotoxic T cells
Are natural killer cells and cytotoxic T-lymphocytes similar in function? I understand that natural killer cells are non-specific and are therefore a part of the 2nd line of defence, however both kinds of leukocytes destroy infected cells, right? They both secrete perforin and destroy cells which display MHC-1-antigen complexes, right? Can someone please clarify the similarities and differences between both cells :)
Yup, they have similar function.  The major difference is NK cells are innate (as you have said) so they don't recognise specific antigens.  NK cells kill without a TCR and without needing to recognise a nonself antigen whereas T cells must recognise a nonself antigen expressed on MHC in order to kill, and T cells have a TCR.
Both the similarities you have listed hold true.
What is MHC?
what is the major histocompatability complex and class 1 + 2 markers?
This excerpt from my notes might help :) -

MHC class I- found on all cells with a nucleus (therefore not red blood cells)
MHC class II- found on professional APCs (antigen presenting cells) like macrophages, dendritic cells and B- and T-lymphocytes.

The major histocompatibility complex itself is a complex of genes that code for MHC (major histocompatibility complex) markers. These markers are unique in every human (excluding identical twins), and are protein molecules which are ultimately located on the surface of cell membranes. They are examples of self molecules.

Foreign antigens as well as self antigens can be displayed on the MHC markers. These can, however, only be peptide antigens. MHC markers can therefore aid in distinguishing between self and non-self.

Cytotoxic T-lymphocytes register MHC I markers
Helper T-lymphocytes register MHC II markers

T-lymphocytes are MHC restricted, whereas B-lymphocytes are not.
What’s the difference between cell-mediated and humoral immunity?
The difference between cell-mediated and humoral immune response..

Would this response be acceptable?
-Cell mediated immune response involves the action of the T Cells whereby T helper cells bind to the antigen fragment on macrophages and activate cytotoxic T cells whereas humoral response involves the production of antibodies against antigens by B Cells
It's too verbose.

The cell mediated response involves T-cells whereas the humoral response primarily involves antibodies, which are produced by B-cells.
Are antibodies produced by B cells or plasma cells?
are antibodies produced by the b cell or the plasma cell? Which one is more correct? My teacher says only plasma cells
When B cells are activated, they differentiate into plasma cells and B-memory cells. Plasma cells produce free-floating anitbodies and release into the bloodstream, they have a pretty short life span.
Are mast cells involved in the inflammatory response?
are mast cells involved in the inflammatory response as well as, the allergic response?

:)
Yes. They are the granulated cells that produce histamines.
Why does subsequent exposure to the same antigen result in a faster and larger immune response?
Why do subsequent exposures to a pathogen generate a greater and faster production of antibodies specific to the antigen? I know that this is primarily due to memory cells, but how/why exactly do they produce a greater and faster amount of antibodies? Wouldn't they have to go through the same process of clonal selection and expansion?
Remember that when a pathogen invade the body for the first time, there is hardly any antibodies in the blood that can combat with that pathogen. It takes the whole process of macrophage engulfing, advertising antigen on its MHCII blah blah blah until that antigen is identified by a B cell and antibodies are produced and that's why symptoms start to occur because it takes a long time. That's the primary response. However, in the secondary immune response, since now you have a larger concentration of antibodies for that specific pathogen inside your body (the antibodies that produced from plasma cells in the previous infection and a large amount of B-memory cells), this process gonna be much quicker, since now your cells have the memory and greater number of cells that can attack that pathogen much more quickly. This is the reason why, after successive immune response to the same pathogen, you might not even realise the symptoms because the large amount of antibodies from the previous infection has already destroyed it.
Just like for the first time, you have 1 machine running to do 1 job, now, you have 100000 machines running just to do the same job.
Can cytotoxic T cells kill cancerous cells? How?
Also, can cytotoxic T cells kill cancerous cells? Cancerous cells would exhibit an abnormal/altered MHC I marker without presenting an antigen fragment, and hence Natural Killer cells would be able to destroy them. However, considering killer T cells activate when they bind to an antigen-MHC I complex of another cell, would this mean cancerous cells are out of the picture?

Edit: I'm pretty sure they can kill cancerous cells, so the question is - how?
Yup, cancer antigens are also considered non-self because they wouldn't have been present in the thymus during T cell development.  Therefore T cells specific for cancer antigens also exist in the naive T cell population and can become activated and form CTL that can kill cancerous cells.  NK cells can also kill them if they have downregulated MHCI, as you have said. So you have two lines of defence against cancer - innate and adaptive :)
The cancer cell expresses the same MHC molecules as what would be present on any other cell but potentially at a reduced frequency.  However, because cancer is caused by a mutation in the genetic material of the cell it might produce abhorrent proteins (antigens) that wouldn't be found in normal cells on those MHC molecules - these proteins are recognised as non-self by the immune system in the context of the same MHC that would be present on noncancerous cells.  It's as if the cell were infected with a virus - presenting the foreign antigen on its surface in the context of MHC, but instead of their being an exogenous agent the cell has just mutated a protein so it is no longer considered 'self'.  Does this make sense?
Why do antibody levels remain higher for a long time after a secondary immune response?
In the secondary antibody response, why does the antibody level remain high for a long period of time after the infection has cleared, in contrast with the primary antibody response in which the antibody level decreases after the infection has cleared?
This is simply a result of having more B memory cells, meaning that it takes longer for them all to deplete.

I mean, it might also be a product of the body's capacity to recognise that subsequent infections reflect the antigen is present in the environment as a consistent threat... But I don't know if that's the case.

You would very rarely be asked to justify this in an exam though. Just know the graph that indicates heightened response and longer term immunity.
Why are antibiotics ineffective against viruses?
Why are antibiotics ineffective against viruses?
Antibiotics generally damage cell membranes, interfere with metabolism or affect cell walls, all of which are not found in viruses.
Can phagocytes detect non-self antigens?
Can phagocytes detect non-self antigens on the surface of pathogens and foreign substances?

Is this what causes them to engulf foreign pathogens in the innate immune response?
Yep, things like macrophages and neutrophils.
What are examples of barriers against food and water borne pathogens?
Barriers against food and water borne pathogens would include stomach pH and digestive enzymes, right? Because they're ingested the pathogens have already 'entered' the body, so the usual defences such as intact skin would surely not be applicable?
Correct. Stomach pH and digestive enzymes are still considered to be in the first line of defence as they are 'external' chemical barriers.
They are external as the gastrointestinal tract is open at both ends.
« Last Edit: November 27, 2018, 02:20:35 pm by PhoenixxFire »
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Re: Biology Q&A archive/Bio FAQ
« Reply #8 on: April 09, 2018, 09:39:33 pm »
+18
U3 AOS 2 Responding to antigens part 2
Relevant study design dot points
• an antigen as a unique molecule or part of a molecule that initiates an immune response including the distinction between non-self antigens, self-antigens and allergens

• invading cellular and non-cellular pathogens as a source of non-self antigens, and preventative strategies including physical, chemical and microbiological barriers in animals and plants that keep them out

• the characteristics and roles of components (macrophages, neutrophils, mast cells, dendritic cells, complement proteins) of the innate (non-specific) immune response to an antigen including the steps in the inflammatory response

• the role of the lymphatic system in the immune response including the role of secondary lymphoid tissue (with reference to lymph nodes) as the site of antigen recognition by lymphocytes, and as a transport system for antigen presenting cells including dendritic cells

• the characteristics and roles of components of the adaptive (specific) immune response including the actions of B lymphocytes and their antibodies (including antibody structure) in humoral immunity, and the actions of T helper and T cytotoxic cells in cell-mediated immunity.

Is microflora part of the 1st line of defence?
Would the normal microflora in humans, considered to be part of the first line of defence?
Yep :)
What is the nature and purpose of MHC?
Need help completing this question:
What is the nature and purpose of the major histocompatibility complex (MHC)?

Any help is much appreciated :)
This is what I know so far:
Firstly, each cell displays each own unique marker on its surface (antigens)
MHC codes for a group of proteins that are found on the surface of cells and these group of proteins are able to differentiate between non-self and self antigens.
If a pathogen comes along, bearing non-self antigens (antigens that doesn't come from the body), then the MHC proteins on a cell (any cell?) will then identify this as foreign as it wont be able to recognize the surface antigens on the cell; thus initiating an immune response.
If a substance comes along bearing self antigens (antigens that comes from the body) then the MHC proteins on a cell (any cell?) will be able to identify this as non-foreign as it will be able to recognize the surface antigens on the cell
Purpose of MHC= to differentiate between non-self and self anitgens
Nature of MHC=  found on all cells?

*there are two types of MHC
- class 1 and class 2

Appreciate any help
Quote
Firstly, each cell displays each own unique marker on its surface (antigens)
MHC codes for a group of proteins that are found on the surface of cells and these group of proteins are able to differentiate between non-self and self antigens.
Okay so this isn't entirely correct. MHC stands for Major Histocompatability Complex. It's a protein found on the surface of all nucleated cells (so all cells except red blood cells). There are two types. MHC1 takes fragments (these are what you called antigens, they are not truly antigens, but VCAA thinks they are) of DNA that is synthesised inside the cell and holds it out into the extracellular fluid.

This is how cell mediated immunity works, Cytotoxic T(Tc) cells attempt to bind to these fragments. Tc cells have a randomly generated specificity (the shape of their binding site is random). During their development, Tc cells that can bind to fragments that are supposed to be made in that person are destroyed (if they are not destroyed, the person may have an autoimmune disease). This means that if a cytotoxic T cell binds to a fragment that is being presented on MHC1, that fragment is not supposed to be there. This means that it is there either because of cancer, a transplant, or most importantly for VCE, a viral infection. None of these things are seen as good, so the Tc cell will kill the cell presenting the fragment. It is also then stimulated to divide and differentiate and cell mediated immunity is triggered.

MHC2 is found on Antigen Presenting Cells (APC's). These are a class of immune cell that includes macrophages and dendritic cells. Macrophages and dendritic cells are also phagocytes. When they find an extracellular pathogen (e.g. a bacteria) they will engulf and destroy it. They then present the antigens that were on the pathogens surface on their own MHC2. A T helper cell will then bind to this and trigger the humoral immune response.

MHC cannot distinguish between self and non self, their only function is presenting antigens or self antigens (DNA fragments).

Quote
If a pathogen comes along, bearing non-self antigens (antigens that doesn't come from the body), then the MHC proteins on a cell (any cell?) will then identify this as foreign as it wont be able to recognize the surface antigens on the cell; thus initiating an immune response.
I've sort of explained this above, the APC (which has MHC 1 & 2) will engulf it (we don't need to know why or how they know its foreign) and then present the antigens on its MHC2. It's a T helper cell that will actually recognise it as foreign by being able to bind to the presented fragment.

Quote
If a substance comes along bearing self antigens (antigens that comes from the body) then the MHC proteins on a cell (any cell?) will be able to identify this as non-foreign as it will be able to recognize the surface antigens on the cell
As above the MHC1 will present the peptide fragments but nothing will happen because no Tc cell will be able to bind to it - they are 'recognised' as self by the lack of reaction. Also a substance won't come along with self antigens on it, the only substance with self antigens will be body cells (that's a bit of an oversimplification but you can think of it like that for VCE).

Quote
Purpose of MHC= to differentiate between non-self and self anitgens
Nature of MHC=  found on all cells?

So the purpose is to present either DNA fragments (MHC1) or antigens from pathogens (MHC2)
I've always though 'nature' question were a bit weird because I was never entirely sure what it's asking but yeah you could probably say its found on all nucleated cells, I would also mention that they're a protein found in the plasma membrane.

Let me know if any of that didn't make sense :)
What is meant by B cell self-tolerance?
What is meant by B cell self tolerance? Where in the body does testing for self-tolerance occur?
I'm not finding any clear answers.
It means that B cells that react to self antigens are destroyed. It occurs during maturation in the bone marrow. When it doesn't happen properly we get autoimmune diseases. T cells are also tested for self tolerance, but for them it's in the thymus.
Hey there.

'Self-tolerance' is a concept that can be attributed to both B cells and T cells, whereby it describes a process where B and T cells are ensured to be non-reactive toward self-antigens. The method through which this is able to occur involves B cells and T cells being exposed to self antigens in specific tissues. If they react to them, they are eliminated (undergo apoptosis etc.), however, if not - then they are considered 'mature naive cells'. These mature naive cells are considered 'self-tolerant' or un-reactive toward self antigens and are able to exit their respective sites of maturation.

In terms of location, this process of maturation occurs in the thymus for T cells (T for thymus) and in bone marrow for B cells (B for bone). I hope this helped.
What pathogens do we need to know about?
Do we need to know about pathogens such as prions, viruses, arthropods, hydatid? What level of detail should we know?
You should know bacteria, viruses and prions quite well - structure, function, etc. I don't really think you need to know arthropods, hydatid to much extent
Prions probably aren't that important tbh. One could make the argument that even the little attention they get in VCE is too much given how rare prion diseases are.
Add fungi to the list as well, should know a bit about them!
Do macrophages present antigens on MHC1 or MHC2?
1: Do macrophhages present antigens on MHC 2 or the MHC 1?
They present antigens from the pathogens they engulf on MHC2. They present antigens that are produced in their own cell on MHC1 (like all nucleated cells do)
How do phagocytes recognise pathogens?
2: How do phagocytes actually recognise pathogens? They don't have antibodies or anything so how do they recognise? Is it their MHC 2 ?
It's probably outside of the course (although 2/3 of the new Biology textbooks talk about this). Phagocytes have a special class of receptors on their surface called PRRs (pathogen recognition receptors). These receptors can respond to a class of molecules called PAMPs (pathogen associated molecular patterns). Basically PAMPs are a small group of molecules that pathogens have, but human cells do not have. A good example of this is the molecule lipopolysaccharide, which is a component of the bacterial cell wall. As human cells don't have cell walls, we don't have lipopolysaccharide. So it makes sense then that this would be a good molecule for phagocytes to respond to, as it can't occur on human cells but does occur on bacteria; meaning that the phagocyte will respond to the bacterium whilst ignoring self cells
Do we need to know about specific pathogens?
Hey guys,

Are we supposed to know specific pathogens for the VCE Biology course? Which pathogens should we know and what level of understanding should we have?

Thanks
Well you should know about the different categories of pathogens - you don't need to know specific examples of ones. You should also have a pretty good understanding about bacteria and viruses, as for prions, fungi, protists, worms etc, you just need to know what they are briefly
What types of cells go under clonal expansions?
Can anyone explain step-by-step how the innate and adaptive immune systems work?
Can anyone explain step-by-step on how innate and adaptive immune system respond to a bacteria and a virus? In order of what happens first please!

Thanks beforehand!
Innate
Okay so the innate system responds the same way to both bacteria and viruses- it's non-specific.

Firstly mast cells release histamine. Histamine binds to capillary walls and causes vasodilation (expansion). This causes more blood to go to the area, which causes heat & redness. Histamine also causes capillary walls to become 'leaky' - white blood cells are able to cross the membrane to access the infected area - this causes swelling.

Some of those white blood cells are phagocytes. Neutrophils are an innate phagocyte. They will travel through the area and phagocytose ('eat') anything that is non-self. Macrophages and dendritic cells are also phagocytes however they are also Antigen Presenting Cells (APC's). They will phagocytose foreign material and then use it to trigger the adaptive immune response.

Also part of the innate immune response are complement proteins.  Complement are actually a group of proteins that perform 3 functions.
1. Aid phagocytosis by opsonizing antigens. Basically they make it easier for phagocytes to find antigens - you don't need to know how.
2. Trigger inflammation by attracting neutrophils and macrophages to the area.
3. Form a Membrane Attack Complex - they make holes in bacterial cell walls.

Because of 3. they are most effective against bacteria.

Humoral (extracellular)
This actually occurs for both bacteria and viruses, but if you get a question on viruses you should talk about intracellular immunity.

Humoral immunity involves B cells, and to a lesser extent T helper (Th) cells.

When pathogens are floating throughout the body, bits of them will inevitably break off. These bits are called free antigens, they will end up encountering a naive B cell that can bind to them. When this happens that B cell is said to be 'selected'.

At the same time a macrophage or dendritic cell that has engulfed a pathogen back in the innate immunity stage will present the antigens from that pathogen on its MHC2 markers. It will then travel to lymph nodes until it finds a naive T helper cell that it can bind to. When this happens that Th cell is 'selected'.

The selected B cell and Th cell travel throughout the body trying to find each other. When they do find each other, the B cell will present the antigen it found to the Th cell. If the Th cell can bind to it then they have the same specificity (they've bound the same antigen). The Th cell will release cytokines (a type of signalling molecule). These cytokines stimulate both the Th and B cell (and cytotoxic T cells in cell-mediated immunity) to divide (make copies) and differentiate (into memory cells and active Th/Plasma B cells). Memory Th and B cells stay in the body to fight against any subsequent infection by a pathogen with an identical antigen. The active Th cells will continue to bind antigens from macrophages and dendritic cells. I'm not entirely sure what the purpose of this continuing is - I believe it has something to do with knowing when to stop the immune response? We don't need to know the details for VCE though Plasma B cells make lots and lots of antibodies with the same antigen specificity (shape of their binding site) as the B cell receptors that bound the initial antigen (these receptors are actually antibodies). These antibodies are released and travel throughout the body binding to any complementary antigens they find.

This has a few purposes.
1. It makes the antigens easier for phagocytes to find.
2. It stops virus antigens from entering cells - it makes them too large
3. It can cause agglutination (clumping). Antibodies have 2 identical receptors so they can bind to two antigens and create a clump.

Cell mediated (intracellular)
Cell-mediated immunity involves cytooxic T cells, and to a lesser extent T helper cells.

This only happens with intracellular infections, as well as cancer, transplantation, and autoimmune responses.

Cytotoxic T (Tc) cells regularly travel throughout the body attempting to bind to peptide fragments presented on MHC1.
MHC1 is found on all cells that have a nucleus - that is, all cells except red blood cells. During normal peptide production, fragments are presented to check that they are self - to check that there is no virus or mutations.

When a Tc cell successfully binds to one of these fragments it is 'selected'. The Tc cell will release granzymes (including perforin) that induce apoptosis in the affected cell. When the cytokines from humoral immunity are released by the T helper cell, the Tc cell will divide and differentiate into memory Tc cells, which remain in the body to kill any cell that presents an identical peptide fragment at a later date and active Tc cells. These active Tc cells will have the same antigen specificity (the same shaped receptor) and will travel throughout the body and kill any cells they find that are presenting the same peptide fragment.
I wasn't really sure what you know so I've probably over explained some parts, let me know if any of that doesn't make sense.
In terms of timing Innate occurs first, adaptive overlaps innnate. Humoral and cell-mediated can start in either order but cell-mediated cannot truly occur until cytokines are released from the T helper cell.

@everyone let me know if I messed any of that up
Do we need to know about plant immunity?
Hey guys,

Do we need to know anything about plant immunity?

Thanks!
Yes, but not that much.
Study design:
• invading cellular and non-cellular pathogens as a source of non-self antigens, and preventative strategies
including physical, chemical and microbiological barriers in animals and plants that keep them out

Plants don't have adaptive immunity, so you just need to know about physical and chemical barriers.
What is an antigen?
Hey can someone please explain to me what exactly antigens are I seem to be very confused? Some sources state it is anything that triggers and immune response whilst others say they are protein markers? Are self-antigens MHC markers found on our cells that identify them as belonging to us whilst non-self antigens are things like pathogens?
Thanks so much.
An antigen is something that can illicit an immune response. Often times they are protein markers on cell surfaces, but they can also simply be molecules of their own.
In response to your question about MHC markers, our own cells posess many different surface antigens. Howeverm as MHC markers are the most important in temrs of the immune system, we mainly focus on these. MHC proteins have two different classes: class I and class II. Class I MHC markers are expressed by all nucleated cells (things like red blood cells don't have them) and present protein fragments from within the cell. As such, these markers can be used to 'check' if the cell is functioning properly as aberrant cells (ie. virus-infected or cancer cells) would produce certain proteins that may be presented to immune cells on these MHC class I markers. MHC class II markers are expressing in certain immunce cells called antigen presenting cells (APCs). This class of MHC marker allows antigens engulfed by the cell to be presented (after processing) on the cell's surface. The main purpose of this is in allowing for activation of the active immune response.
In reguards to non-self antigens, there are many sources of these. Pathogens are one source, as they present and produce molecules that can trigger an immune response. But there are proteins and molecules  - like those of allergens - which can also illicit an immune response that are not pathogenic.
Hope this helps.
Can B cells proliferate & differentiate without a Th cell?
When B cells are selected i.e. when an epitope binds to their receptor, is this process known as clonal selection? And then do they differentiation & proliferate, or do they have to find a corresponding selected T helper cell which would secrete cytokines promoting differentiation & proliferation?
The answer isn't really relevant to VCE, but a really interesting question nonetheless (and as usual!).

B-cells can't differentiate without T-cell help. They can proliferate, but the degree of proliferation is really limited.
Can a person produce antibodies against monoclonal antibodies?
Can the immune system produce antibodies against monoclonal antibodies and how would this work? A prac exam says that eventually an individual will produce antibodies against monoclonal antibodies. How would this work if monoclonal antibodies don't have markers on their surface to display them as foreign?
Some monoclonal antibodies are made out of rat antibodies. The rat antibody is seen as foreign.
What are the roles of complement proteins in the inflammatory response?
1. What are the roles of complement proteins in the inflammatory response?
- I read on Wikipedia that complement proteins attract macrophages and neutrophils, however, I thought cytokines released by the injured cells did this? Can someone please clarify? I also heard they promote inflammation but how does this work? Do they have any other roles?
1. Complement proteins are involved in opsonisation, MAC deposition and chemotaxis (as far as VCE is concerned). Chemotaxis means chemical (chemo) attraction (taxis: to move in response to stimuli). Therefore, complement attracts immune cells to the site of infection in the inflammatory response. The release of cytokines by injured cells also acts to attract immune cells to the site of infection. Different substances can have the same function.
How does the inflammatory response help adaptive immunity occur?
2. How does the inflammatory response help the adaptive immune response occur?
I had the impression they were distinct as the inflammatory response does not retain immunological memory?
2. The inflammatory response is a bridging mechanism between the innate and adaptive immune responses. Specific innate immune cells acquire antigenic fragments and present this to the adaptive immune response’s cells (i.e. Tc cells), this allows for the occurrence of the adaptive immune response.
Why can’t antibodies attack intracellular pathogens?
3. Why are antibodies relatively ineffective at fighting intracellular viral infections?
I can somewhat grasp this concept but am not too sure about it - are they ineffective on intracellular viral infections because they can only bind to foreign antigens and the invaded cell would only have its own normal MHC-I markers? But I thought these cells could display antigens of the pathogen on their MHC-I markers? Or is it because the cells cannot phagocytose the viruses and thus get the foreign antigens displayed?
3. Antibodies function extracellularly, causing; agglutination, opsonisation, neutralisation and complement activation. As viruses intracellularly attack cells, extracellular antibodies are inefficacious against them. (Note: Plasma B cells secrete antibodies into the bloodstream or lymph).
Is there a difference between B cell receptors and antibodies?
Is there a difference between B cell receptors and antibodies?

I assume its just a functional difference; antibodies neutralise antigens, whereas B cell receptors recognise antigens.
Yeah it’s just functional. B cell receptors are just antibodies that are embedded in membranes. Note that antibodies also recognise antigens though. Better to say that they allow differentiation/proliferation to occur by binding their complimentary antigen or something like that.
What's the difference between clonal selection and expansion?
6. What's the difference between clonal selection and expansion?
6. Clonal selection is when a B or T cell is activated. Clonal expansion is when it multiplies producing lots and lots of identical daughter cells.
Are MHC marker only on human cells? Are they on pathogens?
Still a little confused about MHC markers so I wanted to clear something up - are MHC markers only present on human cells or do other pathogens (e.g. virus, bacteria) have MHC markers?
MHC markers are only present in vertebrates, so no, they would not be present in pathogens.
Does the inflammatory response occur even if there is no pathogen?
Hi again...Sorry to keep bombarding the bio question thread, but just wondering, does the inflammatory response, including histamine release, occur only if a pathogen enters the body (e.g. through broken skin), or in all cases, even if there is no pathogen?
No, it's not only if there's a pathogen. It also occurs when you get a cut even if pathogens don't get in. Whenever mast cells are damaged they release histamine, so something like a sprained ankle can also cause inflammation even though there's no pathogen. There's a few different things that cause mast cells to release histamine, but the most common is them being damaged.
Are complement proteins effective against viruses?
Are complement proteins not effective against viruses? If so, why
1.
No they're not really effective against virus'.
The three things they do are:
1. Opsonize pathogens: They stick on the surface of pathogens in the extracellular environment and make it easier for leukocytes to recognise them.
2. Attract phagocytes to the area: They are chemoattractants, phagocytes will be drawn to the source of complement proteins.
3. Create pores in bacterial membranes. Form a Membrane Attack Complex (MAC): They create a hole in the bacteria, causing fluid from the extracellular environment to rush in and rupture the bacteria.
So they're only effective against extracellular pathogens (especially bacteria).
Why is the immune response faster in a secondary exposure than in a primary exposure?
Why is the immune response faster in a secondary exposure than a primary exposure?
2.
This is due to memory cells. During a primary exposure there's one naive immune cell that will recognise the antigen. During a secondary immune response there's lots of memory cells floating around that will recognise the antigen. This means that the antigen will be recognised faster and therefore response will be faster and larger.
What do lysozymes break down?
1) What do lysozymes break down in particular? Is this relevant for VCE biology or should I just know that they are first-line barriers against antigens?
1. They break down a component of bacterial cells walls which causes the cell wall to become unstable and no longer function correctly causing the death of the bacterial cell.
Do we need to know about the parts of an antibody?
Do we need to know about light chains and heavy chains and parts of an antibody for the exam, cos I haven’t really learnt much about that at all  :(
study design:
'the characteristics and roles of components of the adaptive (specific) immune response including the actions of B lymphocytes and their antibodies (including antibody structure) in humoral immunity, and the actions of T helper and T cytotoxic cells in cell-mediated immunity.'

Yes

U3 AOS 2 Immunity

Relevant study design dot points
• the difference between natural and artificial immunity, and active and passive strategies for acquiring immunity

• vaccination programs and their role in maintaining herd immunity for a particular disease in the human population

• the deficiencies and malfunctions of the immune system as a cause of human diseases including autoimmune diseases (illustrated by multiple sclerosis), immune deficiency diseases (illustrated by HIV) and allergic reactions (illustrated by reactions to pollen)

• the use of monoclonal antibodies in treating cancer.

What causes the production of IgE antibodies?
In the allergic response, what actually causes the production of IgE antibodies? these are the steps i have, can somebody please check them??
  • organism is exposed to the allergen for the first time
  • results in the production of IgE antibodies which travel in the blood stream and bind to mast cell
  • mast cells are primed
  • second encounter with the allergen produces IgE antibodies which bind to mast cells
  • results in the release of histamine, resulting in an allergic response
in the second encounter, IgE antibodies are already bound to mast cells - it is the allergen which binds to these specific IgE antibodies, forming cross-links and resulting in the degranulation of histamine by mast cells.
What is hypersensitivity? How does it occur?
Can someone explain to me what hypersensitivity is and how that response occurs?
Body produces IgE antibodies against an antigen that it shouldn't, these IgE antibodies get stuck in the surface of mast cells. Secondary exposure to the antigen activates mast cells by means of the IgE antibodies on the surface, this causes degranulation of mast cells, which results in the release of histamine. Histamine then causes all the inflammation and nastiness related to hypersensitivities.*

*strictly speaking this is not exactly correct, but in the VCE course it suffices.
What’s the point of booster injections?
Lastly, can someone please explain to me everything we need to know about booster injections? I actually have no clue
14. After a time, memory cells start to die off. So you give a booster to create more.
What is a vaccine? What are the different types?
Can someone please give me a definition to vaccine?
And a simplified explanation of all the types of vaccines that are available? (eg attenuated etc.)

Thank you :)
A vaccine is an antigenic substance made from the disease causing agent to provides immunity against that specific disease. It is usually made up of an altered, weakened or killed microorganism or inactivated forms forms of toxins or antigens.

Live attenuated vaccine
Involves a living microbe that has been weakened in the lab, usually through repeated culturing
Inactivated vaccine
Also known as 'killed vaccines', contain microbes inactivated by heat/radiation/chemicals
Subunit vaccines
Dont contain any live microbial components, only haveparts of microbes selected for their ability to induce an adaptive immune response.
Toxoid vaccines
are non-recombinant subunit vaccines that use toxins inactivated by toxoids.
What causes histamine to be released?
1. What are the causes of the release of histamine?
1. There are many causes: Damage to the surrounding tissue, cross linking of bound antibodies (an allergic response), it can also be released by some medicine (including morphine and some antibiotics - but we don't need to know this)
Why do we have IgE antibodies that react to harmless allergens?
2. In the allergic response, the production of (igE) antibodies is stimulated by the entry of an allergen to the body. Does this mean our body contains B cells/antibodies that are specific to and activated by normally harmless antigens? Or only in some people? The initiation of the allergic response when the allergen is identified is confusing me a bit.
2. IgE antibodies bind to mast cells. They only cause the mast cells to degranulate (release histamine) when they cross link (2 antibodies bind to the same antigen) This normally only occurs when a big pathogen is present eg. A worm (parasite). An allergic response occurs when too many IgE antibodies are produced, meaning too many are bound to mast cells, meaning a small allergen eg. Pollen. Can bind to 2 antibodies (as they are located closer together) causing the mast cell to degranulate when it shouldn't.
Not sure about the specificity part, only antibodies against self antigens are destroyed in maturation so it stands to reason that there would be antibodies capable of binding to allergens by random chance.
Why do some vaccines need booster shots?
- why do some vaccines need booster shots?
Some vaccines need booster shots because the number of memory cells decline faster.
Why do allergic responses become worse at subsequent exposures?
- why do allergic response become worse after subsequent exposures to an allergen?

Thank you in advance :)
Allergic responses become worse because each subsequent reaction produces more antibodies against it, which causes a larger reaction at next exposure.
Do IgE antibodies normally bind to mast cells (outside of allergic responses)?
Do IgE antibodies that are not specific to allergens bind to mast cells normally?
All IgE can bind to mast cells, yes.
Difference between active and acquired immunity?
What is the difference to active immunity and acquired immunity, or are they exactly the same thing?
Thanks.
Acquired immunity means that you've become immune to a particular allergen; applies to both passive and active.
There are 3 categories for describing immunity (you won’t see these categories elsewhere I just made them up so it makes more sense). A type of immunity will be able to be described with labels from 1 or more categories, depending on the type (ie. a vaccine will give you artificial, acquired, active immunity).
Category 1: When you receive it
Aquired(Adaptive) immunity=Not born with it
Innate immunity=Born with it
Category 2: Your body’s role
Active immunity=Body produces own memory cells
Passive immunity=Receive antibodies from another
Category 3: How you receive it
Natural immunity=No human intervention. Either get sick or transferred from mother (eg through placenta, breast milk)
Artificial immunity=Given by a human (ie. doctor). A vaccination or injection of antibodies
How might an examination of cells help diagnose disease?
How might an examination of cells help diagnose disease?
Well the form of the cells can often tell you whether or not they're diseased. They will, in many cases, actually appear diseased. Especially cancer cells, which often have multiple nuclei and really jagged edges, for example. Or in sickle cell anaemia, the cells appear to be shrunken and sickle-shaped. Just a couple of examples, but by looking at the cells, often you can see the characteristic signs of certain diseases.
What is the difference between active and passive acquired immunity?
Can someone please differentiate between active and passive acquired induced immunity? Thanks!
Induced active immunity is acquired through vaccination with a dead or attenuated pathogen. The body's immune system responds to the pathogenic antigens by producing specific antibodies against it. The body producing it's OWN antibodies is what makes it active. Since the antibodies are produced by the body, memory of the pathogen is retained (B and T memory cells made)

Induced passive immunity is acquired through injection of antibodies from an external source. The body does not make it's own antibodies and so this immunity is passive. No B or T memory cells are made.
What line of defence is vaccination?
What would immunisation and vaccination fall under? What level of defence?
Third line of defence - they rely on either the provision of a specific adaptive response or the generation of an adaptive response with memory; not permitted by the innate systems in 1st and 2nd line.
How do booster vaccines work?
what are booster vaccines and how do they 'wake up' memory cells? What do the cells do when they 'wake up?'
A booster vaccine is an extra administration of a vaccine after an earlier dose. After initial immunisation, a booster injection is a re-exposure to the pathogen. Its purpose is to increase the individual's immunity against that antigen after a specified period.

After initial exposure, next exposure to pathogen will stimulate T helper cells to stimulate B-cells. B-cells will undergo faster clonal selection and expansion due to previous exposure to pathogen. Booster vaccine creates a stronger and faster response in the production of B plasma cells (and its specific antibodies) and B memory cells.

Essentially, memory of the pathogen is retained and 'boosted' when we have recurring bouts of vaccines.
Are basophils involved in an allergic response?
Are basophils also involved in producing histamines to produce an allergic response?

Thanks!
Yes they secrete the chemical histamine, circulating in the blood and respond to inflammatory and allergic reactions.
Why does the allergic response increase in severity?
Why does the allergic response increase in its severity, with consecutive exposure to the allergen?

Are there more mast cells present each time?
Yes.

So the way an anaphylaxis response works is like so:

Mast cells contain vesicles of histamine waiting to be released.

Upon the 1st exposure of the allergen, antibodies are formed. These then sit on mast-cells with the two variable regions reaching into the extracellular fluid surrounding the cells. These antibodies link with the allergen spread across the two separate antibodies (think   Y-Y) essentially linking them together in a chain.

When they are re-exposed BAM. These antibodies trigger a cascade response, the vesicles are exocytosed and the reaction occurs.

Subsequent exposures may or may not trigger the creation of more mast cells hence increased severity.
The antibody response to the allergen will be greater, but there shouldn't be increased production of mast cells :P
Why does active immunity last longer than passive immunity?
Why is it that active immunity is long-lived whereas passive immunity is short-lived?
- due to presence of memory cells in the body which are able to produce antibodies
Yeh, that seems right - the memory cells allow the long lived nature of active immunity
Passive immunity only involves antibodies not memory cells, these antibodies are used up and then there is nothing left protecting the body whereas active immunity involves antibodies produced by the bodies own immune cells – this means that there are also memory cells. These memory cells are not used up and remain in the body to fight off subsequent infection by a pathogen with the same antigen which is why the immunity is long-lasting.
What do we need to know about monoclonal antibodies?
Could someone briefly explain monoclonal antibodies please? My class was told to just make notes from the Nature of Biology textbook and I'm not sure what we need.

Thanks!
It's new to the study design, so your teacher probably isn't too sure themself.

The study design dot point is very small - it just says that you need to know their role in treating cancer.

Here's what i wrote in my notes about them:

Monoclonal antibodies: Antibodies made synthetically in a lab, they all have the same antigen specificity.

They are made by fusing a plasma B cell that produces antibodies with a desired antigen specificity to a cancerous cell, resulting in a B cell that will divide indefinitely.

If antibodies that were specific to proteins only expressed by cancerous cells could be made, they could travel around a patient’s body and stick to cancerous cells.

These antibodies could be modified to carry things such as radioactive isotopes.
They could be used to set off complement cascades.
A toxin could be attached to antibodies that will be delivered straight to cancerous cells.
Antibodies could be made to stimulate fas R receptors and therefore trigger apoptosis in cancerous cells.
Antibodies could also carry a non-self antigen to allow phagocytes to find the cancerous cells.
Antibodies can also be used to damage blood vessels that lead to tumours (tumours can sometimes cause new blood vessels to form).
Are monoclonal antibodies a form of rational drug design?
Hi,

Can someone explain how monoclonal antibodies work... is it a form of rational drug design?

Thanks,
Rational drug describes how a drug is synthesised against a particular disease/disorder to target a biomolecule, vital in the development of the disease/disorder. (The best example is drug which binds to an enzyme that produces a molecule necessary for the ongoing duration of the disease and inhibits it’s action).

Monoclonal antibodies are artificially synthesised antibodies which complementarily bind to a specific antigen, especially those on cancer cells. It does this by inducing apoptosis on the cell/ flag cells for recognition by other immune cells for destruction/ block binding site.

Although I am unsure whether a monoclonal antibody is a rational drug, I would conclude it isn’t. It is synthesised artificially the same way and do both inhibit the actions of a biomolecule necessary for the development of the disease, however, I would not regard monoclonal antibodies as “drugs” but yet again mocolonal antibodies can deliver radiation or chemotherapy treatment as per NHT VCAA Biology 2018 Paper. I may be wrong so please correct me!
Monoclonal antibodies are antibodies that are produced from a single plasma B cell. Basically, the process is:
   1. An antigen (for which antibodies are required) is injected into the cell of an animal (e.g. a mouse). The animal produces plasma B cells that are specific to the antigen.
   2. The plasma B cells are removed and fused with a tumor cell (called hybridisation) because tumor cells replicate rapidly and uncontrollably, and therefore are very effective to produce high numbers of the plasma cell.
   3. The result is called a hybridoma cell, and it is capable of synthesising large amounds of the monoclonal antibody. They can be extracted and used for theraputic purposes, such as diagnostic tests such as pregnancy tests, neutralising toxins in poisons that are produced by endotoxins in the blood, or to target cancer cells if the body does not do this itself.
I am pretty sure that monoclonal antibodies are not a rational drug, but someone else might have to clarify this.
For VCE rationally designed drugs are only molecules designed to bind to enzymes active sites so monoclonal antibodies definitely aren’t considered a rationally designed drug (for  VCE at least).
How do monoclonal antibodies carry drugs to target cells?
Hi

Does anyone know how monoclonal antibodies carry drugs to target cells?

thanks,
The drug is attached to an antibody. The antibody has antigen binding sites complementary to a molecule associated with that disease. The antibody bonds to that molecule, and the drug is therefore in the right spot.
What are the major uses of monoclonal antibodies?
What are the major uses of monoclonal antibodies?
Also do we need to learn the types and process of designing a monoclonal antibody?
Genetic drift includes the changes in allele frequencies due to chance/random/unpredictable events e.g. a natural disaster (bottleneck effect) or mutations

Well monoclonal antibodies are essentially designed to specificially target one antigen, which may be a specific antigen to a cancer or something relating to the viability of the cancer. Therefore, we can use these antibodies to promote phagocytosis, or maybe conjugate them with a cytotoxic drug to directly deliver it to the cancerous cells to induce apoptosis. There are lots more examples of this. I doubt you need to know how they are made though
Monoclonal antibodies are mainly used for cancer treatment in the scope of our course (as darkz has mentioned)
They are produced by fusing a plasma B cell which produces the antibody of the desired specificity with a tumor cell such that the resultant cells will indefinitely produce extractable antibodies.
The major uses of monoclonal antibodies include their extracted and used for theraputic purposes, such as diagnostic tests such as pregnancy tests, neutralising toxins in poisons that are produced by endotoxins in the blood, or to target cancer cells if the body does not do this itself. All we need to know about, according to the study design, however, is their use for treating cancer cells

It is probably a good idea to have a basic understanding of the process - it is pretty simple to understand.
As you are probably aware, monoclonal antibodies are antibodies that are produced from a single plasma B cell. Basically, the process is:
1. An antigen (for which antibodies are required) is injected into the cell of an animal (e.g. a mouse). The animal produces plasma B cells that are specific to the antigen.
 2. The plasma B cells are removed and fused with a tumor cell (called hybridisation) because tumor cells replicate rapidly and uncontrollably, and therefore are very effective to produce high numbers of the plasma cell.
3. The result is called a hybridoma cell, and it is capable of synthesising large amounds of the monoclonal antibody.

Not sure about the different types, however.
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Re: Biology Q&A archive/Bio FAQ
« Reply #9 on: April 09, 2018, 09:39:57 pm »
+18
U4 AOS 1 Changes in the genetic makeup of a population
Relevant study design dot points
• the qualitative treatment of the causes of changing allele frequencies in a population’s gene pool including types of mutations (point, frameshift, block) as a source of new alleles, chromosomal abnormalities (aneuploidy and polyploidy), environmental selection pressures on phenotypes as the mechanism for natural selection, gene flow, and genetic drift (bottleneck and founder effects) and the biological consequences of such changes in terms of increased or reduced genetic diversity

• processes of evolution including through the action of mutations and different selection pressures on a fragmented population and subsequent isolating mechanisms (allopatric speciation) that prevent gene flow

• the manipulation of gene pools through selective breeding programs.
 
What are missense and nonsense mutations?
Do we need to nonsense and missense mutations?

Yes.
Nonsense-codes for a premature STOP codon.
Missense-codes for a different amino acid.

What does it mean when a gene is highly conserved?
what does it mean when stating that "actin is highly conserved"
Does it mean the gene coding for actin has a low mutation rate?
 
Being conserved means that it remains essentially unchanged throughout evolution.
How did natural selection cause the divergence of humans and chimps?
Chimpanzees are the closest living relative to modern humans (98% of our genomes are similar). Explain in terms of natural selection,  how the two species diverged
Thank you all :D
Okay, so firstly you'll need to consider the principles of natural selection:
-variation of phenotypes present within a population (clines; occur by chance) prior to exposure to selection pressure.
-struggle for survival due to selection pressures (abiotic and biotic)
-selective advantage (favourable phenotypes)
-inheritance (individuals with selected phenotypes reproduce, therefore passing on favoured genes to their offspring)
-frequency of selected phenotypes thus increases within a population (microevolution)

So, when answering the question you'll need to address these principles.
An example of an answer may be:
The divergence would have occurred due to their common ancestor inhabiting different areas and therefore exposing itself different selection pressures. Due to the phenotypic variation within the species, different traits would have been selected for in these different environments. The favoured traits would have then been passed on via inheritance, increasing the frequency of their alleles within the population. This example of microevolution would have eventually resulted in speciation when the gene pools of both groups became isolated so that successful interbreeding could not occur.

My answer is verbose ahah but I think it covers the question :)
What are short tandem repeats (STRs)?
Could someone explain to me what STR(short tandem repeats) are I just don't understand what they are and what they do?
Just repeats of a small sequence of code (2-5bp). So it may just be TATATATATATATATATATATATATATATATATATATATATATATATATATATATATA

So you've got lots of short repeats that are together in tandem. They're mainly in the non-coding regions of DNA. They're useful in pedigree analysis because they're easy to probe and the mutation rate is a little bit higher for these regions. Therefore, they're more polymorphic (more varied) than other sites of the genome.
What’s the difference between translocation and insertion mutations?
What is the difference between translocation and insertion mutations?
Insertion is a copy being inserted into a different DNA segment - the original is still in the correct place as well.
A translocation is the original moving to a different DNA segment - there is only the one copy though.
What is the founder effect?
Does anyone have a simpler explanation of the founder effect? My book is not very clear!
Group of people break off from the population.
Go to a new joint.
Only breed with each other.
-> lower level of genetic diversity.


Example: let's say a mutation occurs in 1 in 1 million people. If 1000 of those people break off and start a new population (isolated from the other) and it so happens that one person in that population has that mutation, you've now increased the prevalence of that mutation to 1 in 1000 in that population.
How does genetic drift/gene flow/selection pressure effect natural selection?
How does genetic drift, selection pressure, and gene flow affect (effect?)/influence natural selection? I've read that it is a changing agent. but I'm not sure how.

Thank you!!
Genetic drift and gene flow change the allele frequencies in a population. They can also introduce a new allele or result in a loss of an existing one. Variation is needed for natural selection to take place.
Selection pressures decide which individuals survive (depending on their phenotype). Those with the favourable characteristic survives to reproduce and pass on their genes to the next generation, increasing the proportion of individuals with that phenotype. This is essentially natural selection.
Genetic drift is a random/chance change in allele frequencies of a population, which may lead to an increase in a certain phenotype (which may or may not be favoured by a particular environment).

Gene flow can rapidly change allele frequencies within a population (due to migration). Genes are exchanged between populations.

Selection pressures are exerted by selective agents which cause differential fitness of certain phenotypes; a certain characteristic (phenotype) is favoured and thus organisms with this certain phenotype have a selective advantage.
Are artificial selection and selective breeding the same thing?
Is 'artificial selection' just synonymous for 'selective breeding'?

Yes, it is.

Through Wikipedia: Selective breeding (also called artificial selection) is the process by which humans breed other animals and plants for particular traits.

Through a university website: Artificial selection (or selective breeding) describes intentional breeding for certain traits, or combination of traits.
How do you define the bottleneck and founder effects?
How would you define bottleneck effect and founder effect?

Thanks.
Bottleneck effect is a decrease in genetic diversity due to a chance event.
Founder effect is when a small, unrepresentative sample leaves a parent population to colonise a new habitat.
Are the bottleneck and founder effects a type of genetic drift?
Would it be correct to say that the founder effect and bottleneck effect are types of genetic drift?
Yes, they are an extreme form of genetic drift.
What is the gene pool?
For this question, the answer is B, but I thought the answer was A... because isn't gene pool the sum total of all alleles, and NOT allele frequencies, so there necessarily doesn't mean great genetic diversity because all alleles could essentially be the same?

If the gene pool of a population is large, this
indicates that:
A there are a large number of organisms in the
population.
B there is extensive genetic diversity in the
population.
C the organisms in the population are fit.
D there is a high chance of extinction.
I think when we talk about the sum of the alleles we talk about the sum of the different alleles. As in if you had a greater variety of alleles the gene pool would be larger regardless of how many individuals there are in that population.
It's actually a combination between A and B that would lead to a large gene pool.
Think about it. A larger number of organisms will not make the gene pool larger, it will only make the population larger. However larger genetic diversity will increase the size of a gene pool as gene pool's consist of the sum of alleles within a population.
Is a disease an example of genetic drift or natural selection?
Hey everyone, would a pathogen wiping out members of a population be genetic drift (since it is a chance/bottleneck event) or natural selection (since only those resistant are selected for survival)?
Well natural selection is a mechanism for evolution that causes a change in allele frequencies due to differential reproductive success in members of a population, whereas genetic drift is a change in allele frequencies due to a random event. Since the hypothetical disease wipes out a subset of the population not randomly, but based on inherent resistance to the pathogen acquired through genetic mutations, it would have to be natural selection.
Why is genetic drift more pronounced in smaller populations?
I’m struggling to understand why genetic drift is more pronounced in smaller populations, could someone explain?
In smaller populations, each individual makes up a higher proportion of all the alleles than in larger populations. In large populations, chance events (such as an individual dying) don't really affect the allele frequency. In smaller populations however, the death of one individual can drastically change the allele frequency. Suppose I had a population in which  50% had genotype RR and the other 50% had genotype rr. In a population of 1000, if one individual were to die, the relative frequency would still be around 50/50. In a population of 2 however, if one individual were to die, then one of the genotypes just gets removed.
I hope this makes sense
What’s the difference between a selection pressure and a selecting agent?
3. Is there a definitive/worth noting difference between selective agent and selection pressure? I've read that they are separate (i.e. a selective agent inflicts a selection pressure on an environment), but when looking for examples of either they usually give the same factors, such as disease or predation. Is there a difference and would anyone be able to demonstrate this with clear examples?
3. It's a technical difference:
Selective agent -the one who enforces the selection pressure eg. Bird, human
Selection pressure - something that favours some individuals over others eg. Predation, hunting
What should we know about aneuploidy/polyploidy/tetraploidy?
What should we know about aneuploid, polyploidy and tetraploidy for the exam?
Pretty sure you just need to know what they are. So know that aneuploidy and polyploidy are types of mutations. Know that monosomy and trisomy are types of aneuploidy. Triploidy and tetraploidy are types of polyploidy etc. you should also know how to write that (so 2n+1, 2n-1, 3n, 4n)
What’s the difference between gene flow and genetic drift?
Can someone explain the difference between genetic flow and genetic drift please? I always get them confused
Genetic flow: changes in the genetic makeup of a population due to individuals moving between populations.

Genetic drift: changes in the genetic makeup of a population due to random individuals dying or not reproducing.

To help remember it:
If something is flowing it’s moving from one place to another (the individuals are moving between populations).

If something is drifting it’s just floating along whichever way it happens to go (the genetic makeup changes due to random deaths).
What’s the cause of genetic differences between species over time?
So over time there are genetic differences between two species.

Are these genetic differences mainly due to mutations or can there be other reasons?
mutations but could also be in addition reproductive isolation (no gene flow between two populations of the same species)
All new alleles are due to mutations however things like genetic drift and selection pressures could change the frequency of alleles or wipe out specific alleles entirely, if this happens differently for each species then they will end up with genetic differences.
Why does natural selection act on phenotypes?
Why does natural selection act on phenotypes?
1. Natural selection is based off how well an individual can survive/reproduce in an environment. It's ability to survive is determined by the traits it has. A phenotype is the traits an individual possesses. Therefore natural selection acts on phenotypes. It doesn't matter whether an individual is heterozygous or homozygous for a trait, it just matters if they have the trait or not.
Does the founder effect always result in speciation?
1) Does founder effect result in speciation always?
1. Not necessarily. The founding population could still be capable of interbreeding with the original population. It just results in lower genetic diversity.

U4 AOS 1 Changes in biodiversity over time
Relevant study design dot points[
• significant changes in life forms in Earth’s geological history including the rise of multicellular organisms, animals on land, the first flowering plants and mammals

• evidence of biological change over time including from palaeontology (the fossil record, the relative and absolute dating of fossils, types of fossils and the steps in fossilisation), biogeography, developmental biology and structural morphology

• patterns of biological change over geological time including divergent evolution, convergent evolution and mass extinctions.

What conditions are required for fossilisation?
What conditions are required for fossilisation to occur?
- Hard objects (such as bone) are more easily preserved
- Rapid burial (protect from scavengers)
- Limited oxygen, water or both
- Abundance of minerals to replace organic substance
- No disturbance of remains so mineralisation can occur

Marine conditions generally suit all this criteria, so that's why there are so many fossils of marine life.
   
Are Index fossils only used for dating?
Are index fossils only used for dating?
Yes, if they use the term 'index fossils' it is referring to dating only, not comparative structure or anything. I asked the same thing.
What does stratigraphy refer to?
Does the term stratigraphy just collectively refer to the principle of superposition and the principle of correlation?
Yes it's just a chronological order of age through startas
Homologous/Analogous structures as evidence for Divergent/Convergent evolution
I know that homologus structures provide evidence for divergent evolution, however, do analogus structures provide evidence for convergent evolution?
Yep, they do :)
Why can’t analogous structures indicate evolutionary relationships?
Why can't analogous structures indicate evolutionary relationships?
Because the structures have different origins (despite having similar functions), therefore they are not related.
Why is potassium – argon dating used for older fossils?
why is potassium-argon dating used for older fossils?
Because Carbon dating has too short a half life (something like 5700 years), so another method is needed for fossils millions of years old.
What’s the difference between divergent evolution and adaptive radition?
I am finding it a bit difficult to understand the difference between divergent evolution and adaptive radiation?
I understand that adaptive radiation is a type of divergent evolution, but is there ever a time when what is occurring/has occurred in a species is only divergent evolution and not adaptive radiation?

Any explanations would be appreciated.
Adaptive radiation is a type of divergent evolution in which the result is a large number of new species being formed to feel niches which may have been emptied in a mass extinction or found in a new environment. Divergent evolution can occur when a species divides to form two or more new species. So if a small number of new species are formed (eg 2 or 3), it is divergent evolution not adaptive radiation. An example of adaptive radiation is the Galapagos finches while an example of only divergent evolution is any species evolving to form two new species.
How do index fossils work?
"Index fossils can provide evidence of the relative age of fossils from different locations".

What does this mean? I know index fossils provide a date for the strata in which they are found in, but how can these fossils be used to provide evidence for the relative age of fossils from different locations?
So index fossils are found in different location and they have a known age. So if you were to find the same fossil(the index fossil) in two different geographical locations you could conclude that those strata have the same age. So if you knew the age of the index fossil you would be able to determine the ages of strata and thus the ages of fossils above and below it. This will allow you to be able to say that X(fossil) is more than Y years old or less the Z years old and by using multiple index fossils or other techniques you would be able to say it is between N years old and M years old.
What is a transitional fossil?
What's a transitional fossil?
A transitional fossil is a fossil that acts as an intermediate between forms.
ie. We have two different species A and C, each having their own fossils respectively. and then one day BAZINGA, we find fossil B, which is an intermediate between the two species. it is a transitional fossil
Why were the oldest rocks found in Canada?
How come the oldest rocks found in Canada not widespread?
They haven't found them elsewhere but that doesn't mean they aren't there. The Earth is a big place. Rock can also undergo metamorphic change that  will stop them from being accurately dated. They just happened to be found in Canada.
How does carbon dating work given the actual bone is replaced by minerals?
1) How can carbon dating be used to date actual fossils if the fossils are replaced by minerals through the process of mineralisation?
1) Carbon dating can only be used on very new fossils (not 'true' fossils) that still have carbon which is why it is not particularly useful.
Are stromatolites a type of trace fossil?
Hi, are stromatolites trace fossils? Or do they actually contain fossilised bacteria? Different sources say different things so I'm a bit confused. Thanks! :D
Stromatolites are chemicals produced by bacteria as a result of metabolic pathways - so they are trace fossils.
What do we need to know about geological history?
HI everyone,
For this dot point in the study design:
-Significant changes in life forms in Earth’s geological history including the rise of multicellular organisms, animals on land, the first flowering plants and mammals.
Do we need to know the different theories (primordial soup theory, RNA world Theory) or do we just need to understand the geological time scale ?
Also, to what extent/ detail should we understand the geological time scale?

Thanks
We can't really be sure exactly what we need to know, but I doubt that you need to know the theories. Given it gives you examples of what events you need to know, just learn them and then generally understand the geological time scale, like how far apart events happened, that complex life developed very recently, etc. You should ask your teacher what they want you to know for your SAC though as they might have a different interpretation of that dot point.
What do we need to know about mass extinctions?
Hi all! What do we need to know about mass extinctions? I understand that is a new topic that has just been added to the study design but the textbook is overwhelming and I just wanted to know what I should learn.
Thanks  ;D
Hey,
Firstly, you should know what mass extinctions are, and then just know a bit about what causes them. I don't think that you need to know specific ones, although that would be beneficial, you probably just need to know the causes of them and their implications.
In convergent evolution, are the species unrelated or distantly related?
With convergent evolution, are the two species completely unrelated or distantly related?
1. technically speaking, no two species are 'completely unrelated' in that they most definitely share some common ancestor whether it be a few a few MYA or as the earliest forms of life. As such I would lean towards saying distantly related, however, I don't know if you would be necessarily marked wrong if you said unrelated.
Can fossils be dated using C14 dating when there is no organic matter remaining?
Can physical fossils be dated using C-14 dating where the original organic matter has decomposed, and the mineralised cast remains? For example like in the case of a fossilised skeleton from 7000 years ago where original bone is unlikely to remain?
Thanks
Nope. Carbon dating is used by measuring the rate at which an organic compound decays - if there’s no organic material left then there won’t be an organic compound there. Carbon-14 dating can be used up to 50000 years, but only if there’s organic material to test.
What’s the difference between divergent evolution and allopatric speciation?
What's the difference between divergent evolution and allopatric speciation?
I've asked my teacher and he said that allopatric speciation is just one source of divergent evolution, but I still don't really understand it - if so, what are the other sources of divergent evolution?
Well divergent evolution describes the pattern in which evolution occurs and is effectively the creation of a new species from an original population e.g. single population of one species becomes two distinct species or possibly more. Therefore, any form of speciation would be considered a source of divergent evolution - there are a few more types of speciation like peripatric, parapatric, and sympatric - but for VCE, you only need to know allopatric speciation
Divergent evolution is the accumulation of differences. Once there are enough differences between two populations they are unable to breed and are therefore different species.

Allopatric speciation occurs when populations are separated by a geographical barrier and accumulate enough differences that they are unable to breed and are therefore different species.

Therefore when a population undergoes allopatric speciation it is evolving divergently.

There are other types of speciation, but you do not need to know about them for VCE.

Edit: Beaten by darkdzn but I’ll post it anyway
In radiometric dating is it the ratio of isotopes or the amount of isotopes being measured?
In radiometric dating, is it the RATIO of the isotopes that is being measured and used to determine the age of a fossil/rock or is it just the amount of an isotope (e.g. in potassium-argon dating, is it the ratio of Potassium-40 to Argon-40 that is being measured and compared to the ratio in new rock, or just the amount of Potassium-40 or Argon-40 created (and no ratio is looked at?) idk if that makes any sense haha
It’s the ratio
What is biogeography?
2) What is biogeography and how does it support the theory of evolution?
Biogeography refers to the range of geographical locations in which fossils and organisms have been found, and are present in. It allows pathways in which organisms have traveled over time to be determined. For example, as the Hominon's moved away from Africa to other locations, such as Asia and then Australia, it can be considered that those found in Indonesia would be more similar to the hominons of Asia than those present of Africa.

Hope this makes sense!

U4 AOS 1 Determining relatedness between species
Relevant study design dot point
• molecular homology as evidence of relatedness between species including DNA and amino acid sequences, mtDNA (the molecular clock) and the DNA hybridisation technique

• the use of phylogenetic trees to show relatedness between species

• the evolution of novel phenotypes arising from chance events within genomes, specifically sets of genes that regulate developmental processes and lead to changes in the expression of a few master genes found across the animal phyla, as demonstrated by the expression of gene BMP4 in beak formation of the Galapagos finches and jaw formation of cichlid fish in Africa.

What does it mean when a gene is highly conserved?
what does it mean when stating that "actin is highly conserved"
Does it mean the gene coding for actin has a low mutation rate?
 
Being conserved means that it remains essentially unchanged throughout evolution.
Why do we measure mutations in mtDNA rather than nuclear DNA?
What would be the advantage of investigating mutation rates in mtDNA rather than nuclear DNA?
Just to clarify a couple of things about mitochondrial DNA:

It is useful as a molecular clock because the mutation rate is known. As far as mutation rate is concerned, the rate of coding sequences is very slow. This is because the selection pressures against mutation in those genes is very strong; cells that accrue mutations in mitochondrial genes will not survive. In non-coding regions, the mutation rate is fast. Slow mutation rate is good because it can show longer term relationships. Fast mutation because it can show short term relationships.

Other bonuses include the fact that there is no crossing over and mitochondrial DNA is, for the most part, maternally inherited.
What is the importance of mitochondrial DNA?
Why is mitochondrial DNA important and what is it used for?
Mitochondrial DNA is passed down the maternal line so can be able to used to identify people in the same maternal line. As mtDNA does not undergo recombination and has very few mutations so can be used to trace back numerous generations. In the mitochondria themselves, they code for proteins needed for cellular respiration.
What is comparative morphology and molecular homology?
In the old study design when it states "comparative morphology; molecular homology" under the subheading of
"evidence for biological evolution over time," what exactly is it referring to?
Comparative morphology is basically comparing structures and the anatomy of two distinct species to determine evolutionary relationships. However, this is not always accurate due to the presence of analogous structures as a result of convergent evolution.

Molecular homology refers to determining evolutionary relationships on the basis of molecular evidence (eg. DNA hybridisation, mtDNA). I think it uses techniques that establish a 'molecular clock' - time taken since two species divergence from common ancestor.
Comparative morphology is the same as comparative anatomy. Essentially, it is studying structures to determine a species' evolutionary past. For instance, homologous structures (like the pentadactyl limb) show two organisms with the same common ancestor, due to a similar structure, and different selection pressures, as the function may be different.

Molecular homology refers to comparing species at a molecular level. So this includes studying: chromosomes, amino acid sequences and DNA sequences through DNA hybridisation etc. (let me know if you want me to further explain any of these and how they are done). Through looking at the amount of differences in each it is possible to see how each species evolved.

Both of these can be used (along with fossil evidence) to develop phylogenetic trees etc to show that evolution must have occured.
Do DNA strands reattach to their own species during DNA hybridisation?
I have a question on DNA hybridisation

Okay so when you have two different organism's DNA and you heat them up to become single-stranded and then mix them up, what stops them from just going back to their exact complementary strand (the same organisms DNA?) - i understand it's the 'mixing' of them but i don't think i get what that actually means.
Excellent question. Shows you're really thinking about what's going on.

You're quite right. Many of the strands will mix with their normal complementary strands; however, many also will not. It's these that you rely on to generate your result :)
What do we need to know about BMP4?
How much and how detailed do we need to know about BMP4 and master genes? There seems to be heaps of questions on this on the prac exams...
From the study design:
• the evolution of novel phenotypes arising from chance events within genomes, specifically sets of genes that regulate developmental processes and lead to changes in the expression of a few master genes found across the animal phyla, as demonstrated by the expression of gene BMP4 in beak formation of the Galapagos  finches and jaw formation of cichlid  fish in Africa.


It is a fairly large dot point but it is mostly about BMP4 as an example of master control genes. I would say you should definitly know:
-What BMP4 does
-That it leads to very fast divergent evolution (called adaptive radiation)
-That mutations occur in the genes coding for regulatory proteins that control its expression NOT in the BMP4 gene itself
-The differences seen due to more/less/early/late in Darwins finches and cichlids

Where exactly do BMP4 mutations occur?

1. Regarding the BMP4 protein/gene (obviously this is new to the study design but I thought I may as well ask if you knew much about it), I read in a textbook that it was a master control regulatory gene, which codes for the protein BMP4, which is a signalling protein that regulates the expression of multiple structural genes that define distinctive characteristics such as beaks, jaws etc. Thus, mutations to the BMP4 gene result in the novel variations of these traits due to altered expression of the BMP4 protein... is this correct? I recently came across a source that said the BMP4 protein was the same in different organisms, hence the mutations did not occur to the BMP4 gene but a different regulatory gene that regulates BMP4 gene expression? I am aware that may not make any sense... but this confused me as it sounded like a regulatory gene regulating a master regulatory gene... If anyone could clarify BMP4 gene, the function of its protein product BMP4, and where these mutations occur, that would be awesome
[/quote]
1. According to Douchy AKA Edrolo guy AKA podcast guy the mutations occur in the gene that regulates expression of the BMP4 gene. Your confusion may be due to textbooks/teachers calling this the BMP4 regulatory gene, but it is not the BMP4 gene.
In DNA hybridisation, does a higher or lower temperature indicate a closer evolutionary relationship?
Hey everyone!
In DNA hybridisation, does a higher or lower temperature indicate closer relatedness between species?
The higher the temperature the more closely related they are.
Species that are more closely related have more matching DNA bases therefore more hydrogen bonds can form, which requires more energy (heat) to break
Why is mtDNA used in molecular homology?
1) Why is mtDNA used in molecular homology? What are the advantages and disadvantages of it?
mtDNA is used as firstly it does not undergo recombination during meiosis. There is alos quite a high yield of mtDNA in cells and also mitochondrial DNA does not undergo the reapair mechanisms that nuclear DNA has. Thus the mutations will accumulate more quickly and substantially in mtDNA, which is important for molecular clocks where they use the rate of mutation accumulation to determine relatedness between species.
What’s the difference between a phylogenetic tree and a cladogram?
Hey guys,

What's the difference between phylogenetic trees and a cladogram? I'm stuck trying to wrap my head around these two.
Cladograms show branching order where the lengths of the branches are meaningless. While phylograms show branch order and branch lengths which mean something (e.g. the number of differences in their nucleotide sequences or time in mya from where they diverged/converged etc)
Are there genes that control BMP4?
1. Are there other regulatory genes that regulate BMP4 genes? My teacher said that BMP4 genes are the top of the hierarchy and thus there are no genes that control it, but how would BMP4 gene be regulated then? (as in how much, when, location, etc.) I also read somewhere on atarnotes where someone said that regulatory genes control BMP4 genes and that mutations occur in these regulatory genes, affecting its expression, so I'm a little confused. With regards to BMP4 as well, I don't think my definition of it is adequate/clear enough, so could someone tell me what I should add or change?: BMP4 is a master gene that produces BMP4 signalling molecule which switches on genes required for cellular differentiation in embryonic (stem?) cells to produce the specific structures of an organism
BMP4 is a regulatory gene that regulates the expression of Bone Morphogenic Protein 4 (also called BMP4)

So mutations in the regulatory gene BMP4 alter the expression of the protein BMP4. It gets super confusing because they’re both called BMP4, but the mutations occur in the regulatory gene BMP4.
« Last Edit: November 27, 2018, 02:21:43 pm by PhoenixxFire »
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Joseph41

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Re: Biology Q&A archive/Bio FAQ
« Reply #10 on: April 10, 2018, 09:12:37 am »
+8
This thread might be the best thing I've seen in my entire LIFE. 😍

EDIT: Many hours later, I still can't even conceptualise how incredible this thread is.
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Re: Biology Q&A archive/Bio FAQ
« Reply #11 on: April 10, 2018, 03:43:58 pm »
+4
*bows down to the ultimate goddess of Biology* 🙇
This is amazing! Phoenixx my gal, you are a lifesaver!!! 🙌
You're both the fire and the water that extinguishes it.
You're the narrator, the protagonist, and the sidekick.
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Re: Biology Q&A archive/Bio FAQ
« Reply #12 on: April 10, 2018, 04:53:40 pm »
+12
This thread might be the best thing I've seen in my entire LIFE. 😍
*bows down to the ultimate goddess of Biology* 🙇
This is amazing! Phoenixx my gal, you are a lifesaver!!! 🙌
Aww thanks guys ❤️

EDIT: Many hours later, I still can't even conceptualise how incredible this thread is.
Oops I broke J41  :P
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Re: Biology Q&A archive/Bio FAQ
« Reply #13 on: April 23, 2018, 05:16:48 pm »
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Re: Biology Q&A archive/Bio FAQ
« Reply #14 on: April 23, 2018, 05:52:42 pm »
+1
You. Are. A. Lifesaver. THANK YOU SO MUCH!  ;D ;D