VCE Biology Question Thread

[PhoenixxFire]

Nope, I was actually talk about the rate of activity
Thank you for the analogy!
A 'rate of activity' is defined as substrates converting into products, so even though you keep on increasing the substrate concentration, yes the amount of enzymes will be occupied with a substrate already, but as soon as an enzyme is finished converting its substrate into a product (this counts as a measure of rate of activity), it moves onto a new substrate, which is why I don't see why the rate of activity would be zero (unless I misconstrued your analogy).

Sorry, a bit hard to explain via text

EDIT: Ok, as I was thinking about it before I posted, I think I understand now.
The rate of reaction (which is the speed of reactants to products) won't actually increase because every enzyme is occupied already, but the amount of products will keep on increasing (I misinterpreted 'rate of activity' as how much reactants turn to products). Unless I'm wrong, please correct me!

Thank you Phoenixxx and Evolio

Yeah the rate of reaction won't be zero, it just won't be increasing any further. Careful with this in the exam, they like to try and trick you by putting things you wouldn't quite expect on the axis of graphs (like, you might expect it to say reaction rate and they'll put amount of product on there instead).

[BitcoinEagle]

Hey guys, some help with a couple questions I have would be AMAZING!
1. What is the full process of protein export? I can only find snippets of the process in my notes.
2. What are the stages of both the humoral and cell mediated immune response?
       Along with this, both B cells and T cells are involved in both parts right? The study design seems to point to B cells being only in humoral and T cells
       being only in cell mediated.

[GFeuilherade]

Hey,
Universal does mean applicable to everything - in bio, universal means that all organisms have the same DNA bases, A T C G and the same structure (a double helix).

Redundant has a similar meaning to unnecessary. In bio it refers to how multiple codons can code for the same amino acid. In order to make a protein, you need to get a chain of the correct amino acids, to get an amino acid you only need one codon that can code for it, so having multiple codons that result in the same amino acid is redundant. You can see this if you look at a codon/amino acid table, the same amino acid will be listed in multiple spots because there are multiple codons that can result in it.

The question asks how an artificial gene can have a different nucleotide sequence (ie different codons) to a human gene, but still produce the same protein (ie the same string of amino acids). This is because DNA is redundant, meaning there are some (many) unnecessary codons that exist within it.

Thanks so much PhoenixxFire! 
🌱🤗

[Comet striker]

Was writing feedback for a practice exam today. But I then got a really interesting question.
Do cancer cells have self antigens? All cells have self antigens on their MHC 1 markers but if your immune system can fight off cancer cells, I'd assume NK and cytotoxic T cells would be involved. How does that stuff work?
Thnx

[sarah15]

Hi! Why is polyploidy common in plants and not animals?

[IThinkIFailed]

Was writing feedback for a practice exam today. But I then got a really interesting question.
Do cancer cells have self antigens? All cells have self antigens on their MHC 1 markers but if your immune system can fight off cancer cells, I'd assume NK and cytotoxic T cells would be involved. How does that stuff work?
Thnx

Haven’t fully revised immunity yet, but I’m pretty sure cancer cells have abnormal self antigens that enable NK cells to bind. Cytotoxic T cells would have a receptor that is specific to one particular type of cancer cell. Both of these cells, when they bind to a cancer cells’ antigen, release perforin to puncture the membrane and degranulate toxins, inducing apoptosis in the cancer cells.

[SmartWorker]

Hi! Why is polyploidy common in plants and not animals?

Polyploidy is often associated with plants, particularly GMOs because they are usually much larger (maybe to provide more nutrient). Whereas, in animals, eg: humans sometimes polypoid cells do appear --> some bone marrow cells are polyploidy.

[Rameen]

Hi everyone,
Are 'technologies for selective breeding' required knowledge for the biology exam.
So like, MOET (multiple ovulation and embryo transfer), sex selection, oestrus synchronisation
The study design says, "the manipulation of gene pools through selective breeding programs"
I'm not sure if that is supposed to cover the technology aspect.

[Evolio]

Yes.
cytotoxic and helper T cells are seperate things. They both already exist in your body as naive Tc and Th cells. A Tc cell will be selected when it finds a cell presenting a fragment it can bind to, a Th cell will be selected when it is presented with a fragment from an APC. When that Th cell is costimulated by a B cell that has also bound a fragment, the Th cell with release interleukins, these interleukins are what causes all the differentiation and proliferation amongst B, Th, and Tc cells. Don't worry too much about remembering the precise details, you probably won't need to talk about Th cells helping Tc cells to divide and differentiate in the exam (but you might need to talk about them helping B cells do that).

Ok.
But where do T memory cells come from?

[PhoenixxFire]

Was writing feedback for a practice exam today. But I then got a really interesting question.
Do cancer cells have self antigens? All cells have self antigens on their MHC 1 markers but if your immune system can fight off cancer cells, I'd assume NK and cytotoxic T cells would be involved. How does that stuff work?
Thnx

Self antigens are protein fragments. During maturation immune cells are exposed to these fragments and any that react are killed.
Cancer cells will produce some self antigens, they will also produce some fragments which will be recognised by immune cells because they aren't ones that they should be making - this is what will trigger the immune reaction against them (in the same way that a protein fragment created by virus DNA will). The self antigens on cells aren't just sitting there for the whole cells life, the cell will stick out different fragments as it's producing them to be checked. Self antigens aren't any one specific thing, they're just fragments that immune cells can't* respond to (as any that did respond were killed.

*with the exception of autoimmune diseases.

Hi everyone,
Are 'technologies for selective breeding' required knowledge for the biology exam.
So like, MOET (multiple ovulation and embryo transfer), sex selection, oestrus synchronisation
The study design says, "the manipulation of gene pools through selective breeding programs"
I'm not sure if that is supposed to cover the technology aspect.

Nah you won't need to know specific technologies, just the general idea of what selective breeding is and how it affects gene pools.

Hey guys, some help with a couple questions I have would be AMAZING!
1. What is the full process of protein export? I can only find snippets of the process in my notes.
2. What are the stages of both the humoral and cell mediated immune response?
       Along with this, both B cells and T cells are involved in both parts right? The study design seems to point to B cells being only in humoral and T cells
       being only in cell mediated.

1). mRNA is transcribed at ribsomes embedded in the rough endoplasmic reticulum, some processing occurs in the rER, the polypeptide then travels via vesicle to the golgi apparatus where more processing occurs, it then gets put in another vesicle which takes it to the plasma membrane to be exocytosed. You don't need to know the details of what happens to it in the rER/golgi apparatus.

2.

humoral immunity

Humoral immunity will be activated:
-A naïve B cell will bind to a free antigen.
-A Th cell will be presented with its antigen on a MHC2 molecule by an APC (macrophage or dendritic cell).
-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.
-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.

cell mediated

-Naïve 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 cause 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 or differentiate until cytokines are present.
-When cytokines have been released from the 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 as the original cell.

It's all connected. If cell mediated immunity is going on, then humoral immunity will be too (but not necessarily the other way around). B cells are only directly involved in humoral immunity, Cytotoxic T cells are only in cell mediated immunity. Helper T cells are involved in both, but they're more important to talk about in relation to humoral immunity.

But where do T memory cells come from?

There's two types of T memory cells - Helper and cytotoxic. They come about in the same way that B memory cells do. When a cell is selected it divides and differentiates to form two different types of cells - memory cells, and the active cells which will fight the current infection.

[Evolio]

There's two types of T memory cells - Helper and cytotoxic. They come about in the same way that B memory cells do. When a cell is selected it divides and differentiates to form two different types of cells - memory cells, and the active cells which will fight the current infection.

Thank you for your help, PhoenixxFire! 

I also have some questions from the 2014 Exam Short Answer.
In question 12 a, they said to define a selection pressure and I wrote:
'A selection pressure is a condition that allows the individuals with advantageous traits to have a higher chance of survival.' Is this an appropriate definition?
Also, they said to give an example of a selection pressure with reference to the information they gave us and I said a spear was a selection pressure as humans used it to kill mammoths. However, the examiner's report said humans( who wielded the spear) but I thought this would be the selective agent?
I hope this makes sense.

[PhoenixxFire]

I also have some questions from the 2014 Exam Short Answer.
In question 12 a, they said to define a selection pressure and I wrote:
'A selection pressure is a condition that allows the individuals with advantageous traits to have a higher chance of survival.' Is this an appropriate definition?
Also, they said to give an example of a selection pressure with reference to the information they gave us and I said a spear was a selection pressure as humans used it to kill mammoths. However, the examiner's report said humans( who wielded the spear) but I thought this would be the selective agent?
I hope this makes sense.

You need to say "environmental condition" and have a comparison. Higher chance of survival than what?

The spear is just a tool. The selection pressure would be hunting, and the selective agent humans. I'd just refer to both (ie say "humans hunting") because VCAA doesn't distinguish between them.

[BitcoinEagle]

Brilliant, thanks so much for the help PheonixFire
I just had 3 more question which should be shorter and easier to answer?
1. What is the point of the untranslated region on DNA strands?
2. What ist he point of the methyl cap and poly-A tail as part of post-transcriptional modifications
3. This is the big one: What is the point of ATP and NADP and how do we define their function?

[ssillyssnakes]

Brilliant, thanks so much for the help PheonixFire
I just had 3 more question which should be shorter and easier to answer?
1. What is the point of the untranslated region on DNA strands?
2. What ist he point of the methyl cap and poly-A tail as part of post-transcriptional modifications
3. This is the big one: What is the point of ATP and NADP and how do we define their function?

I know I'm not who you asked, but I hope I can be of help

1. The purpose of introns are a little bit vague (and is definitely not needed to know for VCE). Some help to code for some RNA molecules, whilst the exact purpose of others is still debatable. The presence of introns does help to facilitate alternative splicing (i.e. how we can have many different proteins from a single gene sequence) but whether this is their initial PURPOSE is not really known as far as I'm personally aware.

2. The methyl cap and poly A tail have two different functions. The methyl cap essentially allows for the mRNA to bind to  undergo translation, making the molecule stable. It also prevents enzymes within the cytosol from damaging/breaking down the mRNA. The poly A tail also helps in preventing the degradation of mRNA from enzymes within the cytosol. The poly A tail also has a role in signalling to the ribosome that the process of translation should be terminated.

3. Molecules like ATP, NADH, and NADPH are known as carrier molecules. Essentially, they help to give energy to allow for reactions to occur. They do this as the process that forms them requires energy (to turn ADP into ATP requires energy) when a process then needs energy, a carrier molecule can donate its energy (for instance, when ATP becomes ADP, it 'gives off' the energy that it absorbed when it became ATP). This means that 'pure' energy can essentially be used by the cell at anytime as long as there are carrier molecules present, allowing for a TON of reactions to happen that otherwise wouldnt/would occur VERY slowly

I hope this helps

[PhoenixxFire]

Brilliant, thanks so much for the help PheonixFire
I just had 3 more question which should be shorter and easier to answer?
1. What is the point of the untranslated region on DNA strands?
2. What ist he point of the methyl cap and poly-A tail as part of post-transcriptional modifications
3. This is the big one: What is the point of ATP and NADP and how do we define their function?

1. Untranslated regions are on mRNA strands (no DNA is translated). They're involved in regulation. The bit upstream of 5' helps with binding and initiating translation, the bit downstream of 3' helps with terminating translation. You don't need to know about it though. There's also non coding regions on DNA, some of which becomes transfer, ribosomal, and regulatory RNAs, some of which is involved in DNA replication, and a fair bit of which has an unknown function. You don't need to know about that either though.

2. The poly-A tail is essentially a timer. The mRNA will break down over time, the longer that poly A tail is the longer it'll take for the actual strand to disintegrate. The methyl cap has a similar function on the other end protecting from endonucleases and it also has a few other functions such as helping with translation. In terms of VCE, just knowing that they help prevent the mRNA from degradation by endonucleases is enough.
It seems I'm too slow today but given I've already written this you can have two answers haha