VCE Biology Question Thread

[smamsmo22]

Okay, lots of stuff here.. good questions.

1. Now, the first point, it is true that THE gene that regulates the expression of the BMP4 gene undergoes mutations to give rise to the novel phenotypes and NOT the BMP4 gene itself... if you look at this from a logical standpoint it makes perfect sense:
- A mutation in the BMP4 gene itself would NOT alter its level of expression, however, would alter the BMP4 protein... resulting in it having a different primary structure and concomitantly a different tertiary structure. This would change or eradicate its functionality (which obviously is not occurring in cichlid fish OR the Galapagos finches).
- Instead, a master regulatory gene that REGULATES the expression of BMP4 is altered, resulting in differential expression of the BMP4 gene, producing the novel phenotypes associated with beak width/depth, and the jaw of cichlid fish (short, heavy etc.).....

2. For the second question, if we consider an allergic response, an allergen or antigen enters the body of an individual, is engulfed and digested by phagocytes, of which then being presented to naive B and T cells... these cells, therefore, to react with the antigen or allergen must have complementary receptors toward it.. whereby producing IgE in response. As far as if only some people have it or everyone has cells with specific receptors to the allergen... I honestly couldn't say (sounds like a question beyond the scope of the course.. but I am sure that with some research online you'd find something!).

Thankyou!
With the first answer, since you've referred to the gene that regulates BMP4 gene as the master regulatory gene; is the BMP4 gene itself also a master regulatory gene, as it is referred to as a master gene in the study design?

[smamsmo22]

Some more thoughts on the question:

Potentially VCAA would accept average or raw as long as you can justify it.

The question asks you about valid conclusions. This implies that they reflect what the “true” answer is. If you use the average, I would argue that you can’t do that because your conclusion would be “there is no change in the percentage of oxygen therefore respiration does not occur”, which is wrong.
However, if you use the raw data your conclusion would be the opposite. In all bar one group, the concentration of oxygen decreased therefore respiration occurred.

You can see clearly that group 2 is an aberration. This is useful information, because it tells us that groups 1, 3 and 4 tell a different story. If you took the average, you lose that vital information.






VCAA have never asked a question like this before, so it’s hard to tell where they’ll go on this. PhoenixFire’s point is compelling and, critically, references the knowledge you need to have; however, common sense dictates that raw is better and on that basis I think it should be correct.

I think I'll trust you and go with raw and give a justification. Thanks for the clarification!

[vox nihili]

Thank you for your answers!! Just a couple of follow up questions for clarification;
1. So now I understand that the mutations to the regulator gene for the master gene BMP4, are what alters the expression of BMP4 protein (not the actual makeup of the protein) and hence produces novel phenotypes. (Thanks!) Am I still correct in saying BMP4 gene is a master control regulatory gene, and that BMP4 protein is a transcription factor that is able to regulate the expression of a suite of structural genes? i.e. there is another regulatory gene (that mutates) that regulates expression of the master regulatory gene BMP4, that regulates the expression of phenotypes?

2. I think I understand the triggering of the allergen of an allergic response, I am just confused about how the initial production of IgE antibodies against the allergen comes about (sensitisation, I should've called it) when it enters the body. I was just confused by the concept that we had B cells that contained/produced specific antibodies against normally harmless allergens? Is that right? And how this only occurs in some people.
Thanks so much!

1. That's correct. Really tricky point, so well done.
2. Yep, you're right. It's basically just your typical B-cell response, except that it's directed against an inappropriate antigen. Your question about why some people develop this and others don't is an insightful one. The reality is, we don't know! This is an area of fairly intense research at the moment.

I think I'll trust you and go with raw and give a justification. Thanks for the clarification!

It's definitely worth discussing with other people and getting their views. Even though I've probably got the most experience in Biology around here, this is a new course and sometimes the VCE course is a little bit idiosyncratic, so I won't always be correct.

[smamsmo22]

Another question that arose while correcting a practice exam (Insight);
The question basically asked about how a new virus strain could come into existence and this was the recommended answer;
"An existing strain of influenza mutates to create a new strain. Genetic drift occurs gradually, and this eventually changes the surface proteins or antigen of the virus. Human immune systems do not recognise the new antigen and treat it as a new infection."
This all makes sense to me except for the part about genetic drift. Unless it's an error and it should be something along the lines of natural selection, I really don't understand how genetic drift contributes to a new phenotype arising from a mutation... If anyone could explain (or clarify if there's a likely error), that would be great!

[PhoenixxFire]

Genetic drift occurs gradually, and this eventually changes the surface proteins or antigen of the virus.

Genetic drift would definitly not cause new surface proteins as only mutations are a source of new alleles (however this could just be bad wording as they mention mutations earlier). All genetic drift could do is eliminate some phenotype by chance. Natural selection is a more likely way for a new strain to arise but genetic drift could cause a new one to arise.

Remember though that the new surface proteins will always be due to mutations.

[ezferns]

I think they might be referring to antigenic drift instead of genetic drift!

[grestal]

PCR: you should already know how that works, so I won’t go into the details. You just get a body sample and see if you can amplify bacterial/viral DNA by using primers specific to that DNA.
ELISA: again, won’t go into too many details. Basically what you do is you get antibodies specific to a pathogen and put them on a slide. Then you get a sample from somebody’s body. If the pathogen is present, the pathogen will bind to the antibodies and will light up (don’t worry about how this works).
Culture: get a sample, chuck it on a dish and see if bacteria grow. This is by far the most common for bacteria, whereas PCR or ELISA are used more for viruses.

thank you!

[Seno72]

Is it required to know ELISA? It doesn't state in the study design.

[LifeisaConstantStruggle]

You might need to know ELISA as an example of a way one detects pathogens, (bacteria) but that's about the most detail you require. (you might wanna know the general procedure for a brief description of it, nothing too detailed so dw)

[TheBigC]

Thankyou!
With the first answer, since you've referred to the gene that regulates BMP4 gene as the master regulatory gene; is the BMP4 gene itself also a master regulatory gene, as it is referred to as a master gene in the study design?

Yes it is indeed also a master regulatory gene... However, I forgot to mention in my previous comment, mutations CAN occur in the BMP4 gene itself, however, to ALTER expression, it must occur in the promoter region..

[PhoenixxFire]

Yes it is indeed also a master regulatory gene... However, I forgot to mention in my previous comment, mutations CAN occur in the BMP4 gene itself, however, to ALTER expression, it must occur in the promoter region..

They can occur but they are generally selected against because BMP4 is so important a small change can have massive consequences (imagine a Galapagos finch without a beak)

[LifeisaConstantStruggle]

They can occur but they are generally selected against because BMP4 is so important a small change can have massive consequences (imagine a Galapagos finch without a beak)

In fact, mutations in the BMP4 gene ALWAYS occur, but these mutations (like what Phoenixxfire has said, are often selected against), and those who have a mutation in the BMP4 gene itself usually die before they're born.

[smamsmo22]

Sorry for all the questions (I had sent these to another source but they haven't gotten back to me so I thought I might as well send these here!) and thanks for anyone who replies!!
1. The study design mentions knowing the major trends in hominin evolution including structural, functional and cognitive changes, and I've been having a bit of trouble differentiating traits into these categories. For example; is increased brain size a structural or cognitive change? And are actions such as migration and tool making considered functional, (not cognitive)?
2. The study design asks for the source and mode of transport of various signalling molecules, including pheromones. I understand how pheromones diffuse through the air, but found a few different answers for their source. So I wanted to know, where are pheromones produced... or where are they emitted from (is there are general answer I could use)?
3. Also in the context of using plasmids to transport foreign DNA into eukaryotic organisms. Are the recombinant plasmids directly inserted into our germ line and/or somatic cells and are functional? Do they somehow get inserted into our chromosomes to be transcribed like our other genes? When asked to describe how they are used to insert genes into our cells I don't really know how to explain this.
4. Concerning block mutations; I've repeatedly read/written that these mutations do not result in any loss of DNA from the organism, however one of the block mutation type is a deletion. If there is a block deletion that arises in a chromosome, can it be assumed that the deleted selection is present on the other chromosome (as a duplication perhaps)?

Thanks for the help!! I hadn't used AN to ask questions before so clearly I've got a few that have piled up whilst studying...

[LifeisaConstantStruggle]

Sorry for all the questions (I had sent these to another source but they haven't gotten back to me so I thought I might as well send these here!) and thanks for anyone who replies!!
1. The study design mentions knowing the major trends in hominin evolution including structural, functional and cognitive changes, and I've been having a bit of trouble differentiating traits into these categories. For example; is increased brain size a structural or cognitive change? And are actions such as migration and tool making considered functional, (not cognitive)?
2. The study design asks for the source and mode of transport of various signalling molecules, including pheromones. I understand how pheromones diffuse through the air, but found a few different answers for their source. So I wanted to know, where are pheromones produced... or where are they emitted from (is there are general answer I could use)?
3. Also in the context of using plasmids to transport foreign DNA into eukaryotic organisms. Are the recombinant plasmids directly inserted into our germ line and/or somatic cells and are functional? Do they somehow get inserted into our chromosomes to be transcribed like our other genes? When asked to describe how they are used to insert genes into our cells I don't really know how to explain this.
4. Concerning block mutations; I've repeatedly read/written that these mutations do not result in any loss of DNA from the organism, however one of the block mutation type is a deletion. If there is a block deletion that arises in a chromosome, can it be assumed that the deleted selection is present on the other chromosome (as a duplication perhaps)?

Thanks for the help!! I hadn't used AN to ask questions before so clearly I've got a few that have piled up whilst studying...

1) Increasing cranial capacity is a structural change (remember, they generally don't explicitly talk about brain size because you have no brains to compare/investigate with), cognitive changes would be abilities such as tool making, or language, abstract and complex thought, social behaviour, things like that. Functional changes include the implications of structural changes, eg: opposable thumb=precision grip, tool making, etc. (note that most of these changes may overlap, and are not fixed into one category.)
2) pheromones are produced in different parts of an organism (depending on its species), for example: a mammal can produce pheromones through the nose (VNO), while an insect can detect pheromones released from their sexual organ to attract mates, there are too many sites of production for us to be able to generalise it into 1 short umbrella term (you don't need this for the exam, just the function of it)
3) It depends on luck really, people just *hope* that their DNA is inserted correctly into the cell's nuclear material (by chance, through a gene gun, pronuclear microinjection, or even a retrovirus) and pray after that.
4) I'm not sure about this one tho...? I apologise for my limited bio knowledge.

Edit: on the pheromones question (2), you can just say stuff like "pheromones produced/secreted by an organism", it should be sufficient for VCE (I've read through VCAA assessor's reports and they don't ask for the sources of the pheromones). But if you're interested, Wikipedia and simple.wikipedia.org will have your back

[vox nihili]

I think they might be referring to antigenic drift instead of genetic drift!

Just to clarify, I’m not sure that antigenic drift is assessable on the VCE biology SS, in case anyone is freaking out

Cool concept though!