VCE Biology Question Thread

[sweetcheeks]

But that doesnt really include the ratios of which the genotypes/phenotypes will show up in
If you account for that, 12/16 wouldd have the H allele so wouldnt A make sense?

I think something has been lost along the way. You do a test cross by breeding an individual (in this case heterozygous) with a homozygous recessive individual. The results I listed will be in a 1:1:1:1 ratio. If possible, could you show your working?

[AhNeon]

I think something has been lost along the way. You do a test cross by breeding an individual (in this case heterozygous) with a homozygous recessive individual. The results I listed will be in a 1:1:1:1 ratio. If possible, could you show your working?

Aight my bad. I just realised that it was a test cross. Misread the question and hence though that it was 2 heterozygotes being crossed.
Thanks for the help!

[FatimaEl]

Hi guys, does anyone know if the 2013 vcaa exam was relatively easy or hard in comparison to all the other years?

[alastair.98]

Hi guys, does anyone know if the 2013 vcaa exam was relatively easy or hard in comparison to all the other years?

I found the multiple choice section to be easy. As for the short answer, I wouldn't say it was one of the more difficult exams but somewhat easy

[FatimaEl]

I found the multiple choice section to be easy. As for the short answer, I wouldn't say it was one of the more difficult exams but somewhat easy

Yes i found the multiple choice to be easy, but the short answer was sort of difficult

[homosapien]

How can the same gene result in different proteins being produced in terms of transcription factors/ regulator genes

[Gogo14]

How does biogeography support evolution?

[HasibA]

How does biogeography support evolution?

if certain species are spread out across the world, and they all have different characteristics, wouldn't that show evidence for divergent evolution, whereby a common ancestor spread out across a lot of land, and diff, selection pressures affected the species.

also, where an organism is found (biogeography is the distribution of plants and animals around the world, and the study of that??) could show how organisms develop and evolve in respect to their environment, mainly due to selection pressures!

i think- correct if wrong

[vox nihili]

1. -The symptoms of asthma are caused in part by the binding of cytokines IL-4 and IL-13 to their respective receptors.
-Dupilumab is able to bind to the IL4-receptor chain alpha, which is found in both of the aforementioned receptors.
-The binding action of Dupilumab to these protein chain alters the binding site of these receptors, resulting in the cytokines being unable to bind to their receptors, and thus the introduction of these monoclonal antibodies into the body may lessen the symptoms of asthma.

2. Monoclonal antibodies against the IL-4 protein chain alpha may be produced by injecting these proteins into a non human organism, such as mice. In doing so, the protein fragments would be recognised as non self in the organism they were introduced into. Thus, specific antibodies would be produced against it in large numbers. These antibodies could then be extracted and then be refined for human use.   

I have no idea how relevant/accurate any of this is, but I tried to answer this as I would a VCAA question, I have found the answer to their questions are usually simple and relatively uncomplicated, which is what I tried to do here

1. Your answer to number one is pretty spot on the money. Don't dismiss the possibility that the antibodies could be acting as a competitive inhibitor, however! Antibodies are really huge molecules and are actually really good competitive inhibitors because they cover so much surface Really good answer though, just adding in the extra info!

2. Your answer to number two is exactly what I was looking for. This does not describe the entire process of making monoclonal antibodies (of course it doesn't!) but it's exactly what you'd be expected to know in VCE and also shows a good understanding of the concept of self vs non-self. Really well done

Not sure any of this actually says anything, but yeah
1. Dupilumab acts as a competitive inhibitor to the cytokines IL-4 and IL-3, binding to the IL-4 and IL-3 receptors. Thus, the binding of these cytokines is decreased and therefore the effects of asthma are also decreased.
2. Mice are injected with the antigens and produce antibodies against it. The plasma cells are taken from the mice and mixed with tumour cells to create hybridomas. The hybridoma cells that make the desired antibody are then cultured to produce large amounts of it.

1. That's pretty spot on the money. Asthma is an allergic disorder. IL-4 in particular plays a really key role in the allergic response; so by blocking it, asthma can't really develop

2. I suspect Google may have helped a little with this one :p Funnily enough though, this isn't actually how dupilumab is made—it's a bit more complicated than the old way they made murine antibodies!

Ok here's another shot
1. Dupilumab has complementary binding sites to IL-4, which is a cytokine, presumably histamine. As a result of binding to this cytokine, the antibody inhibits its function by agglutination of IL-4 hence preventing circulation of the cytokine around the body. As a result, allergic side effects like inflammation and swelling is decreased.
2. Genes for Production of human antibodies are inserted into another animal via a recombinant plasmid. The animal then produces this monoclonal antibody and the antibodies are collected for use.
Not sure if half of what I said was relevant, Lol

1. You're right in pursuing the theme of the antibody being complementary to something and thereby inhibiting it, but once again you need to be really careful about how you read the question. The question stated that dupilumab binds the IL-4 receptor chain alpha, which is a shared component of the IL-4 and IL-13 receptors. Dupilumab doesn't bind IL-4 at all, it binds its receptor. Binding its receptor essentially has the same effect though; it prevents IL-4 from signalling to cells

2. A good answer and a completely reasonable one in these circumstances. What I was trying to suggest was that you could inoculate a mouse (this is just a wanky way of saying inject) with IL-4 receptor chain alpha and—because it's a human protein and not a mouse protein—the mouse will produce an immune response against it. Specifically, the mouse will produce antibodies specific to the IL-4 receptor chain alpha.

Your idea about making recombinant antibodies is not a bad one though. To get the specificity to the IL-4 receptor chain alpha, you do need to do as I described above; however, after this what we tend to do now is extract the genes producing antibodies from the B-cells specific to this protein and express these in bacteria as you described. By doing this we can actually fiddle with the genes and take out some mousy bits and replace them with humany bits (so that we don't have an immune response to the antibody!).


FEEDBACK TO EVERYONE

Really pleased with all of your ideas here guys! As I said, this question was meant to be harder than you would cop in a VCAA exam. You shouldn't feel dismayed if you didn't manage to answer it; all of your ideas were valid and showed that you think really well.


Dupilumab is actually a fairly cool drug. It has really improved treatment of asthma for a small section of asthmatics who have really severe, intractable asthma. In these people, standard treatments for asthma fail to do very much for them, so I'm sure you can appreciate how much it means to them to have a treatment that actually controls their asthma well

PS: monoclonal antibodies will be on the new course!

[instax101]

With this question, why isn't the answer A? (it's B by the way)

Since it's an original plasmid, wouldn't it be cut by restriction enzymes to make space for the desired gene? So 5.3-2.9 and then + 2.9 for the gene, making it 5.3kb again?

[couchpotato]

(Image removed from quote.)

With this question, why isn't the answer A? (it's B by the way)

Since it's an original plasmid, wouldn't it be cut by restriction enzymes to make space for the desired gene? So 5.3-2.9 and then + 2.9 for the gene, making it 5.3kb again?

The desired gene is going to be inserted into the plasmid, a plasmid that does not contain the desired gene originally.

So instead of 5.3-2.9, it's more you are inserting the desired gene (2.9) into the plasmid (5.3) resulting in a fragment that is 5.3+2.9= 8.4 long. That's why the answer is Lane 3.

[HasibA]

The desired gene is going to be inserted into the plasmid, a plasmid that does not contain the desired gene originally.

So instead of 5.3-2.9, it's more you are inserting the desired gene (2.9) into the plasmid (5.3) resulting in a fragment that is 5.3+2.9= 8.4 long. That's why the answer is Lane 3.

doesnt 8.4 long mean lane 4 or am i jus silly

[instax101]

The desired gene is going to be inserted into the plasmid, a plasmid that does not contain the desired gene originally.

So instead of 5.3-2.9, it's more you are inserting the desired gene (2.9) into the plasmid (5.3) resulting in a fragment that is 5.3+2.9= 8.4 long. That's why the answer is Lane 3.

Yes I understand that, but in order to make a recombinant plasmid don't you need a restriction enzyme that creates sticky ends to cut the plasmid? If not, then you're completely missing the step here.

Unless I'm missing something, that is

[sweetcheeks]

Yes I understand that, but in order to make a recombinant plasmid don't you need a restriction enzyme that creates sticky ends to cut the plasmid? If not, then you're completely missing the step here.

Unless I'm missing something, that is

You are correct, you do need a restriction enzyme. However, this enzyme does not remove any genetic material, it simply makes an incision into the plasmid.

I will use a watch analogy. You have a watch that has a steel band composed of multiple links. The watch is a bit tight so you decide you want to add a couple more links. You do this by separating the links at a point (restriction enzyme) and you add in more links. None of the old links were removed but new ones were inserted. The band is now going to be larger than it initially was.

[instax101]

You are correct, you do need a restriction enzyme. However, this enzyme does not remove any genetic material, it simply makes an incision into the plasmid.

I will use a watch analogy. You have a watch that has a steel band composed of multiple links. The watch is a bit tight so you decide you want to add a couple more links. You do this by separating the links at a point (restriction enzyme) and you add in more links. None of the old links were removed but new ones were inserted. The band is now going to be larger than it initially was.

That makes so much sense thank you so much!