VCE Biology Question Thread

[IThinkIFailed]

Thank you!
I just notice infected cells can't travel to the lymph nodes. Yep, APC place them on both markers but cytotoxic T cells bind to MHC-1 makers.

But does this mean could the cytototic cells react against the APC since it is also displaying a foreign marker?

Oh I think I get what you mean now, my bad, I forgot that APCs also have MHC 1 markers, and yea, I’ve researched a bit, and APCs can actually present antigens on their MHC 1 markers to cytotoxic T cells. Of course, the cytotoxic T cells don’t actually differentiate until a specific T-Helper cells secrete cytokines. I wouldn’t say that infected self cells can’t travel to lymph nodes. In fact, cancer cells can actually end up in lymph nodes, and if they aren’t killed by Tc cell’s, can cause cancer within the lymph nodes.
Just a question, when defining homologous structures e.g : homologous structures refer to different species that have structures that have bones arranged in the same underlying pattern, indicating common ancestry.

Would you mention that the structures would have different functions, or is that too specific?

Mod edit (PF): Merged post. Please edit your post rather than posting twice in quick succession

[ssillyssnakes]

Just a question, when defining homologous structures e.g : homologous structures refer to different species that have structures that have bones arranged in the same underlying pattern, indicating common ancestry.

Would you mention that the structures would have different functions, or is that too specific?

I wouldn't mention it when defining homologous structures generally, but if the question was referring to a particular instance where species' had homologous structures with different functions, then it would be good to mention that

[IThinkIFailed]

I wouldn't mention it when defining homologous structures generally, but if the question was referring to a particular instance where species' had homologous structures with different functions, then it would be good to mention that

Thanks for the help!

Another question, what is a good definition of a gene pool?
I’ve come across this kind of question quite a few times while doing practice exams, and the best one I’ve come up with is:
Sum of alleles in a population. I feel this is a bit too basic though...

Also, is this a good description of the steps of DNA hybridisation? The brackets are indicating stuff I’m not sure if I should include or not
1: Source double stranded DNA from The cells of two different species (and purify the samples)
2: Heat the samples to 95 degrees Celsius, denaturing the DNA and causing them to disassociate into single strands
3: Mix the (single stranded) samples from both species, allowing the complementary bases of each strand to pair
4: Heat the sample of the two species, and compare with how much heat it took to denature the DNA samples of double stranded DNA from each species. (The closer the temperature to this point, the higher the degree of complementary base pairing and thus less diffferences in their nucleotide sequences)

[ssillyssnakes]

Thanks for the help!

Another question, what is a good definition of a gene pool?
I’ve come across this kind of question quite a few times while doing practice exams, and the best one I’ve come up with is:
Sum of alleles in a population. I feel this is a bit too basic though...

Also, is this a good description of the steps of DNA hybridisation? The brackets are indicating stuff I’m not sure if I should include or not
1: Source double stranded DNA from The cells of two different species (and purify the samples)
2: Heat the samples to 95 degrees Celsius, denaturing the DNA and causing them to disassociate into single strands
3: Mix the (single stranded) samples from both species, allowing the complementary bases of each strand to pair
4: Heat the sample of the two species, and compare with how much heat it took to denature the DNA samples of double stranded DNA from each species. (The closer the temperature to this point, the higher the degree of complementary base pairing and thus less diffferences in their nucleotide sequences)

The best and most concise definition I can find for a gene pool is "the complete set of alleles present in a population" which is what is defined by VCAA. I dont think that you'd get marks taken off for substituting alleles with genetic information either. As long as it mentions genetic traits within a population it should be fine.

In relation to DNA hybridization, your description is fairly good, if not too specific (depending on how many marks a question is worth, of course) although I would mention that when the two samples of denatured DNA are mixed, the solution is cooled to allow for the complementary sections of DNA to form hydrogen bonds and anneal. Other than that, great job!

[nianid]

Hey guys I just finished the 2018 Biology exam and I was wondering how many marks i would get for this answer for Q6c

BMP4 gene is a regulatory gene that controls the rate of expression of the signalling protein BMP4 during embryonic development of the Galapagos finches. Different levels of expression of BMP4 protein across different species of finches lead to variation of beak size and length with larger expression of BMP4 protein leading to bigger and broader beaks due to longer expression of BMP4 gene. Variation of beak sizes in different finches population allows for a variety of phenotypes to arise for natural selection to occur.

The examinor's report makes it sound as if BMP4 gene is a structural gene but I thought it was regulatory? Thanks!

[ssillyssnakes]

Hey guys I just finished the 2018 Biology exam and I was wondering how many marks i would get for this answer for Q6c

BMP4 gene is a regulatory gene that controls the rate of expression of the signalling protein BMP4 during embryonic development of the Galapagos finches. Different levels of expression of BMP4 protein across different species of finches lead to variation of beak size and length with larger expression of BMP4 protein leading to bigger and broader beaks due to longer expression of BMP4 gene. Variation of beak sizes in different finches population allows for a variety of phenotypes to arise for natural selection to occur.

The examinor's report makes it sound as if BMP4 gene is a structural gene but I thought it was regulatory? Thanks!

I'm fairly sure that BMP4 is indeed a structural gene, and the level at which it is expressed is controlled by other regulatory genes. So, for instance, in the case of the Galápagos finches, the gene coding BMP4 isn't different between the different finches, but rather what differs between them is the rate at which BMP4 is translated, so the mutation occurs  a regulatory gene that contributes to that rate of synthesis.

There are many others on here that know much more than I do, so if anything I've said is wrong, please correct!

[IThinkIFailed]

Hi guys, I’m a bit unsure about my steps for the hydrophilic signalling molecule signal transduction pathway
Here are my steps:

1: Hydrophilic signal binds to complementary receptor, causing a conformational change in its 3D shape so that secondary messengers are activated
2: Secondary messengers activate a cascade of events (amplifying the signal)
3: Cascade of events activates effector molecules

The step I’m a bit unsure about is 3, I don’t know whether I should say “effector molecules” or say that the cascade of events relays the signal to the nucleus.

If you see any other issues with my process, please criticise it and tell me!
Thanks

[ssillyssnakes]

Hi guys, I’m a bit unsure about my steps for the hydrophilic signalling molecule signal transduction pathway
Here are my steps:

1: Hydrophilic signal binds to complementary receptor, causing a conformational change in its 3D shape so that secondary messengers are activated
2: Secondary messengers activate a cascade of events (amplifying the signal)
3: Cascade of events activates effector molecules

The step I’m a bit unsure about is 3, I don’t know whether I should say “effector molecules” or say that the cascade of events relays the signal to the nucleus.

If you see any other issues with my process, please criticise it and tell me!
Thanks

Your answer is pretty good, the one thing I would clarify would be at the end of step 3 adding that the activation of the effector molecule results in a specific response by the cell.

For most questions you dont need to do into the specifics of the conformational change of the receptor to the extent that you have (just saying that it results in a conformational change in the receptor molecule is fine) but you certainly won't lose marks for that

[Erutepa]

Hi guys, I’m a bit unsure about my steps for the hydrophilic signalling molecule signal transduction pathway
Here are my steps:

1: Hydrophilic signal binds to complementary receptor, causing a conformational change in its 3D shape so that secondary messengers are activated
2: Secondary messengers activate a cascade of events (amplifying the signal)
3: Cascade of events activates effector molecules

The step I’m a bit unsure about is 3, I don’t know whether I should say “effector molecules” or say that the cascade of events relays the signal to the nucleus.

If you see any other issues with my process, please criticise it and tell me!
Thanks

I agree completely with ssillyssnakes above, but just want to add that for hydrophilic signal transduction, it doesn't necessarily relay the signal to the nucleus. The signal may illicit a cellular response that does not involve altering gene expression, in line with the function of hydrophilic signalling molecules to illicit faster acting more immediate responses (since altering gene expression takes some time)
Altering Gene expression is instead more so associated with hydrophobic signaling molecules which typically cause longer lasting responses such as in modulating cell development

[PhoenixxFire]

does the activation of cytotoxic T cells include binding to APCs and T helper cells releasing cytokines or can it be that it binds the infected cells and T helper cells release cytokines.

Is this definition correct?
- APCs engulf pathogen and place the foreign antigens on its MHC-1 and 2 marker.
- Cytotoxic T cells binds to corresponding antigen on the MHC-1 marker using their T cell receptor
- Cytokines are secreted by activated T helper cells that actives the cytotoxic T cell and cause it to differentiate and proliferate into active cytotoxic cells and memory cytotoxic T cells.
-The active cytotoxic T cells travels around the bodies and recognise specific antigen presented on the MHC -1 makers of infected cells
- When it bind to the antigen, it recognise it as foreign and secretes granzymes and perforins that rupture the plasma membrane causing it lysis and die.

APC's do have both MHC1 and MHC2, however the only antigens presented on MHC1 are protein fragments synthesised by the cell - so antigens that are engulfed are only presented on MHC2, not MHC1.

APC's can present antigens on their MHC1 to Tc cells, the same way any other cell can, but this will kill the APC because it signals that the APC is infected. APC's can also present on MHC2 to activate T helper cells, which is why they're called APC's.

The cytokines released from Th cells when they come into contact with an activated B cell with the same antigen specificity are required for Tc cells to divide and differentiate, however VCAA considers Th and B cells as part of humoral immunity, and Tc cells as part of cell mediated immunity. So if you get a question on cell mediated immunity, it's okay to mention that the Tc cells are stimulated by cytokines released from activated Th cells, but you won't need to go into any sort of detail on it, save that for the humoral immunity questions.

Hi guys, I’m a bit unsure about my steps for the hydrophilic signalling molecule signal transduction pathway
Here are my steps:

1: Hydrophilic signal binds to complementary receptor, causing a conformational change in its 3D shape so that secondary messengers are activated
2: Secondary messengers activate a cascade of events (amplifying the signal)
3: Cascade of events activates effector molecules

The step I’m a bit unsure about is 3, I don’t know whether I should say “effector molecules” or say that the cascade of events relays the signal to the nucleus.

If you see any other issues with my process, please criticise it and tell me!
Thanks

In addition to what other said, make sure you specify that it's a membrane bound receptor. Also for 3. I'd also mention that the cascade of events leads to a cellular response.

If you don't mind me asking, what were those general events for the timeline?

this is what vcaa said about it

Question: Are students required to know dates for the changes in life forms in Earth’s geological history, and which specific life forms should be considered?
Answer: No, although specific dates are not required students should understand geological
time is divided into sections, for example eras and periods.
Students should understand that Earth’s history can be represented on a geological time scale
as a ‘calendar’ of chronological events: different kinds of organisms do not appear randomly but appear in a constant order as the law of fossil succession. The fossil record shows the changes that have occurred in the types of organisms living over time.

Also, is this a good description of the steps of DNA hybridisation? The brackets are indicating stuff I’m not sure if I should include or not
1: Source double stranded DNA from The cells of two different species (and purify the samples) You don't need this line
2: Heat the double stranded DNA samples to 95 degrees Celsius, denaturing the DNA and causing them to disassociate into single strands
3: Mix the (single stranded) samples from both species, allowing the complementary bases of each strand to pair You need to say that the solution is cooled down which allows the strands to bond. They'd probably already be mixed together during heating.
4: Heat the sample of the two species, and compare with how much heat it took to denature the DNA samples of double stranded DNA from each species double stranded hybird dna. The higher the temperature required, the more closely related the species are. (The closer the temperature to this point, the higher the degree of complementary base pairing and thus less diffferences in their nucleotide sequences)

[Evolio]

Hey guys!
I just had some questions from the 2009 exam 1.

1c.
I said that the function of cholesterol is to maintain fluidity in the cell membrane. Is this correct? VCAA said that cholesterol increases the fluidity of the cell in colder temperatures

2 c i
Is it correct if I say tRNA is found at the ribosome?

2 c ii
In translation, is it correct to say that tRNA carries a complementary amino acid to the codon on the mRNA? Also, would it be correct to say that tRNA carried a complementary anticodon? Like can we use anticodon and amino acid interchangeable when referring to translation? Like, aren't they referring to the same thing? Do we have to talk about amino acids and anticodons?

3 c
The question asked for what was the purpose of additional pigments and I said that it is able to trap and aborb different coloured light and VCAA said to 'trap and absorb different wavelengths of light'? Is my answer correct?

3 e
So, according to the graph provided, does high light intensity along with high temperature denature enzymes? Does this mean that high temperature and low light intensity does not denature enzymes? This is referring to photosynthesis by the way.

7 e
In autoimmune response, is it basically the same as normal immune response with pathogen except autoantibodies are produced instead? Like does agglutination still occur and the B cells being activated by T helper cells and self antigen being presented to T helper cell by antigen presenting cell?

8 a
B cells mature in the bone marrow
B cells are produced in the bone marrow.
Do these two statements mean the same thing?

[ssillyssnakes]

Hey guys!
I just had some questions from the 2009 exam 1.

1c.
I said that the function of cholesterol is to maintain fluidity in the cell membrane. Is this correct? VCAA said that cholesterol increases the fluidity of the cell in colder temperatures

2 c i
Is it correct if I say tRNA is found at the ribosome?

2 c ii
In translation, is it correct to say that tRNA carries a complementary amino acid to the codon on the mRNA? Also, would it be correct to say that tRNA carried a complementary anticodon? Like can we use anticodon and amino acid interchangeable when referring to translation? Like, aren't they referring to the same thing? Do we have to talk about amino acids and anticodons?

3 c
The question asked for what was the purpose of additional pigments and I said that it is able to trap and aborb different coloured light and VCAA said to 'trap and absorb different wavelengths of light'? Is my answer correct?

3 e
So, according to the graph provided, does high light intensity along with high temperature denature enzymes? Does this mean that high temperature and low light intensity does not denature enzymes? This is referring to photosynthesis by the way.

7 e
In autoimmune response, is it basically the same as normal immune response with pathogen except autoantibodies are produced instead? Like does agglutination still occur and the B cells being activated by T helper cells and self antigen being presented to T helper cell by antigen presenting cell?

8 a
B cells mature in the bone marrow
B cells are produced in the bone marrow.
Do these two statements mean the same thing?

I'm going to try my best to answer these, but I can't say I'm certain on everything.

1.c) Cholesterol does maintain fluidity, meaning that it doesn't just CAUSE the plasma membrane to be fluid, but also prevents it from becoming TOO fluid, like in really hot environments where otherwise the phospholipids composing the PM would 'break apart' - cholesterol prevents that and makes sure the PM is perfectly fluid, but not too fluid.

2.c.i) That's difficult to say whether or not that would be accepted by the examiners. Technically,  tRNA is found in the cytosol of the cell, it isnt WITHIN the ribosome, but it delivers amnio acids to the ribosome. I'm not entirely sure whether saying that tRNA is found at the ribosome would be correct.

2.c.ii) I would personally say corresponding amino acid rather than complementary, because complementary kind of implies that only one codon codes for one amino acid, which, given the redundant nature of the genetic code, isn't exactly correct. I don't think the tRNA necessarily CARRIES the complementary anticodon, but is rather just composed of the complementary codon - if that's incorrect someone please correct me. Finally, the anticodon and amino acid don't mean the same thing and I wouldn't use them interchangeably. The anticodon is like the 'key ' that tRNA binds with the codon to, which allows for tRNA to release the corresponding amino acid.

3.c) I would generally say wavelengths of light, not colours. Whether or not colours of light would be accepted in an exam really depends on the examiner, but the safest bet is to try and always use the term wavelengths of light

3.e) Light intensity doesnt denature enzymes, from what I can find, it is just temperature which does, as a high light intensity just results in faster photosynthesis (up to a point, when no more light can be absorbed - but that doesnt cause any damage to the cell or proteins). Low light intensity with high temperature would denature proteins.

7.e) This is something I am also not entirely sure about, and hopefully someone else can further clarify. I believe that autoimmune diseases cause for a cell to be marked as non self, and thus the attack would be the cell mediated response (as the 'problem' is intracellular) - so complementary cytotoxic t cells would be produced and kill the cells. Again, I may be wrong, and if so please someone else correct me.

8.a) The statements don't mean the same thing. B cells are produced in the bone marrow, however I'm fairly sure they mature in secondary lymphoid tissue.

Hope that helps

[Erutepa]

Hey guys!
I just had some questions from the 2009 exam 1.

1c.
I said that the function of cholesterol is to maintain fluidity in the cell membrane. Is this correct? VCAA said that cholesterol increases the fluidity of the cell in colder temperatures.

Cholesterol does maintain the fluidity of the cell membrane (increasing fluidity at low temps + decreasing fluidity at high temps). I personally don't think you would be marked wrong for this, but perhaps it would help if you specified the specific changes in fluidity in higher/lower temperatures.

2 c i
Is it correct if I say tRNA is found at the ribosome?

tRNA can be found occasionally at the ribosome during translation, however, the better response would be in the cytoplasm/cytosol where it hangs about waiting to bind to mRNA at the ribosome.

2 c ii
In translation, is it correct to say that tRNA carries a complementary amino acid to the codon on the mRNA? Also, would it be correct to say that tRNA carried a complementary anticodon? Like can we use anticodon and amino acid interchangeable when referring to translation? Like, aren't they referring to the same thing? Do we have to talk about amino acids and anticodons?

tRNA does carry a complementary amino acid to the ribosome. tRNA doesn't carry an anticodon as such - tRNA has site known as the anticodon which is complementary to a specific codon. This complementarity between the anticodon and the codon facilitates the binding of the tRNA to the mRNA and this allows for specific amino acids to be delivered to the ribosome as dictated by the codons of the mRNA.
 - the amino acid is the molecule that the tRNA carries (each tRNA is specific to an amino acid)
 - the anticodon is a region on the tRNA composed of 3 nucleotides complementary to a specific mRNA codon

3 c
The question asked for what was the purpose of additional pigments and I said that it is able to trap and absorb different coloured light and VCAA said to 'trap and absorb different wavelengths of light'? Is my answer correct?

You might get the mark for this, but I think it might be best to use the term wavelength in the future.

3 e
So, according to the graph provided, does high light intensity along with high temperature denature enzymes? Does this mean that high temperature and low light intensity does not denature enzymes? This is referring to photosynthesis by the way.

This question is wanting you to identify different limiting factors of the rate of photosynthesis. For the low light intensity plants, the rate of photosynthesis remained relatively low and constant, not because enzymes were denatured, but because the rate of photosynthesis was limited by the low light intensity itself. You can still see that as the temperature approached 40 degrees, the rate dropped sharply, indicating that denaturation of enzymes did still occur.
In the case of the plants with the higher light intensity, the lower temperatures acted as a limiting factor initially (reducing the frequency of collisions) and as the temperature increases, the rate of photosynthesis increased until denaturation occurred.
Remember that denaturation will occur regardless of light intensity.

7 e
In autoimmune response, is it basically the same as normal immune response with pathogen except autoantibodies are produced instead? Like does agglutination still occur and the B cells being activated by T helper cells and self antigen being presented to T helper cell by antigen presenting cell?

Autoimmune responses are the exact same.
While not in the course (sadly - as it is fascinating), your body produces immune cells (B and T cells) that can mount immune responses to essentially any convincible protein, however in normal individuals, the immune cells that respond to self-antigens are killed during their development (to put it simply) and only the immune cells that respond to foreign antigens remain. However, in the case of autoimmune disorders, this process doesn't occur properly and some immune cells that respond to self-antigens survive and mount immune responses against self in just the same way a normal immune cell would respond to a foreign antigen. You DO NOT need to know this, however it might help understand a bit about autoimmune diseases.

8 a
B cells mature in the bone marrow
B cells are produced in the bone marrow.
Do these two statements mean the same thing?

No.
While you don't really need to understand the maturation process, you need to be able to state that B cells are produced in the bone marrow and mature within the bone marrow also. By contrast, T cells are produced in the bone marrow but migrate to and mature in the Thymus.
____________________________________________________________________

I'm fairly sure that BMP4 is indeed a structural gene, and the level at which it is expressed is controlled by other regulatory genes. So, for instance, in the case of the Galápagos finches, the gene coding BMP4 isn't different between the different finches, but rather what differs between them is the rate at which BMP4 is translated, so the mutation occurs  a regulatory gene that contributes to that rate of synthesis.

There are many others on here that know much more than I do, so if anything I've said is wrong, please correct!

Just to correct this a little bit, BMP4 is, in fact, a regulatory gene, coding for the protein BMP4, which is a signalling molecule which alters gene expression. In Galapagos finches, the quantity and timing of BMP4 expression determine the size and shape of the finches beaks formed.
The precise description (relative to the Galapagos finches and cichlid fish) given by VCAA from the 2018 Examiner's report is:
Galápagos finches: The BMP4 gene is a gene for a signalling protein that is responsible for
beak formation in Galápagos finches. The longer the gene is expressed in the embryo, the more
BMP4 and the larger the beak that develops. This allowed diversity in beak shape and length in
populations of finches and different phenotypes for natural selection.
African cichlid fish: The BMP4 gene is responsible for jaw formation in African cichlid fish. When
BMP4 is overexpressed in the embryo, it can change the jaw shape. This allowed diversity in
jaw shape and length in populations of cichlids and different phenotypes for natural selection.

[ErnieTheBirdi]

Hey everyone, my AOS3 Unit2 Sac is tomorrow and I was just wondering whether anyone had any tips to just do some last minute revision to prepare myself. The SAC is a report writing one. Thanks everyone !

[ssillyssnakes]

Cholesterol does maintain the fluidity of the cell membrane (increasing fluidity at low temps + decreasing fluidity at high temps). I personally don't think you would be marked wrong for this, but perhaps it would help if you specified the specific changes in fluidity in higher/lower temperatures.tRNA can be found occasionally at the ribosome during translation, however, the better response would be in the cytoplasm/cytosol where it hangs about waiting to bind to mRNA at the ribosome.tRNA does carry a complementary amino acid to the ribosome. tRNA doesn't carry an anticodon as such - tRNA has site known as the anticodon which is complementary to a specific codon. This complementarity between the anticodon and the codon facilitates the binding of the tRNA to the mRNA and this allows for specific amino acids to be delivered to the ribosome as dictated by the codons of the mRNA.
 - the amino acid is the molecule that the tRNA carries (each tRNA is specific to an amino acid)
 - the anticodon is a region on the tRNA composed of 3 nucleotides complementary to a specific mRNA codonYou might get the mark for this, but I think it might be best to use the term wavelength in the future.This question is wanting you to identify different limiting factors of the rate of photosynthesis. For the low light intensity plants, the rate of photosynthesis remained relatively low and constant, not because enzymes were denatured, but because the rate of photosynthesis was limited by the low light intensity itself. You can still see that as the temperature approached 40 degrees, the rate dropped sharply, indicating that denaturation of enzymes did still occur.
In the case of the plants with the higher light intensity, the lower temperatures acted as a limiting factor initially (reducing the frequency of collisions) and as the temperature increases, the rate of photosynthesis increased until denaturation occurred.
Remember that denaturation will occur regardless of light intensity.Autoimmune responses are the exact same.
While not in the course (sadly - as it is fascinating), your body produces immune cells (B and T cells) that can mount immune responses to essentially any convincible protein, however in normal individuals, the immune cells that respond to self-antigens are killed during their development (to put it simply) and only the immune cells that respond to foreign antigens remain. However, in the case of autoimmune disorders, this process doesn't occur properly and some immune cells that respond to self-antigens survive and mount immune responses against self in just the same way a normal immune cell would respond to a foreign antigen. You DO NOT need to know this, however it might help understand a bit about autoimmune diseases.No.
While you don't really need to understand the maturation process, you need to be able to state that B cells are produced in the bone marrow and mature within the bone marrow also. By contrast, T cells are produced in the bone marrow but migrate to and mature in the Thymus.
____________________________________________________________________Just to correct this a little bit, BMP4 is, in fact, a regulatory gene, coding for the protein BMP4, which is a signalling molecule which alters gene expression. In Galapagos finches, the quantity and timing of BMP4 expression determine the size and shape of the finches beaks formed.
The precise description (relative to the Galapagos finches and cichlid fish) given by VCAA from the 2018 Examiner's report is:
Galápagos finches: The BMP4 gene is a gene for a signalling protein that is responsible for
beak formation in Galápagos finches. The longer the gene is expressed in the embryo, the more
BMP4 and the larger the beak that develops. This allowed diversity in beak shape and length in
populations of finches and different phenotypes for natural selection.
African cichlid fish: The BMP4 gene is responsible for jaw formation in African cichlid fish. When
BMP4 is overexpressed in the embryo, it can change the jaw shape. This allowed diversity in
jaw shape and length in populations of cichlids and different phenotypes for natural selection.

Thank you for that, I looked into it a bit further after your explanation and that makes a ton of sense!