VCE Biology Question Thread

[cosine]

In general I've found Unit 3 exams to be a lot harder than unit 4 exams. Is anyone like this?

Im the opposite, im struggling immensely with unit 4 exams, its mainly the whole evolution part... ah..

The secondary structure is a result of hydrogen bonding between backbone functional groups (carboxyl and amide). Tertiary structure can be a consequence of inter-sidechain functional group hydrogen bonding (or what I'm awkwardly trying to say, there are functional groups in the protein in places other then the backbone that aren't involved in secondary structure.)

Is it essential to mention backbone functional groups when describing the secondary structure? Can we just say secondary structure is the result of  hydrogen bonding between the functional groups (carboxyl and amine) between amino acids within the polypeptide chain. Or must we include the backbone?

[Mishmosh]

Hey guys

I hope someone can answer these questions

If carrier proteins are specific to the molecules they can move across the membrane then why can they change shape?
Are channel or carrier proteins used for active transport?
Where does the link reaction occur?
Are there any factors that limit the rate of cellular respiration?
Which organ releases ADH?
Is clotting of the blood first or second line of defence?
What is an opportunistic infection?
How does the body destroy multicellular parasites?

Thank you

[vox nihili]

No. No. No. Maybe? (no) No.

Fail on my part, sorry all

Don't know why I even hang in this thread lol think it just happened by mistake... my knowledge of the finer or past-VCE points of Biology is, well, shaky, and until I do the biomed degree I yearn for but will never do, I'll only lead y'all astray

One wise word of advice that this proves, before taking a graceful exit from this thread: to score highly, you can actually be amazingly ignorant.  I didn't score sensationally or anything, but I knew far less even than I do now in year 12 (like really basic things, like I didn't know what a leading/lagging strand or Okazaki fragments were, or that B cells can't proliferate without TH cells), and still pulled a 45 raw.  If you make sure you know all the solid basics, then you'll score more highly than you imagine because the depth VCAA expects you to know things is surprisingly shallow

So take heart and make sure you know those solid basics!

Don't be silly, you do a really good job on this thread. When I was first posting in first year I got a few things wrong; hey, I do sometimes now and that's after three years of biology.

I've got to admit too, I had to look up the primer thing the other day hahaha

Is it essential to mention backbone functional groups when describing the secondary structure? Can we just say secondary structure is the result of  hydrogen bonding between the functional groups (carboxyl and amine) between amino acids within the polypeptide chain. Or must we include the backbone?

Pretty sure you can just list the secondary structures. You don't have to directly reference the backbone amide or carbonyl groups.
You would technically be wrong saying that it's caused by hydrogen bonding between functional groups. This is also involved in tertiary structure.

Hey guys

I hope someone can answer these questions

If carrier proteins are specific to the molecules they can move across the membrane then why can they change shape?
Are channel or carrier proteins used for active transport?
Where does the link reaction occur?
Are there any factors that limit the rate of cellular respiration?
Which organ releases ADH?
Is clotting of the blood first or second line of defence?
What is an opportunistic infection?
How does the body destroy multicellular parasites?

Thank you

They have to change shape to pull them across the membrane. Proteins are dynamic, just because something changes shape doesn't mean that they lose their specificity. Recall the difference between lock-in-key and induced fit. Lock-in-key is actually a really poor way of describing the interaction between an enzyme and its substrate. It's also a poor way of describing the interaction between a carrier protein and its substrate. Induced fit is better. Upon binding, the protein and the substrate will both change structure, because the molecular interactions involved in binding pull on each of them and that moves elements of the molecules around.

Carrier proteins are used for active transport.

I have no idea what that is.

Too many to count. Cellular respiration has to be regulated. For instance, when one exercises, the rate of respiration in muscle cells increases dramatically.

I wouldn't even really consider it as part of the immune system. You wouldn't be asked.

You don't need to know. They're infections that occur when the immune system is compromised. A robust immune system would otherwise prevent them from occurring.

Much in the same way they destroy unicellular pathogens. (there are some differences in the response but this is well beyond the VCE course)

[StupidProdigy]

Should I know anything about diabetes, insulin and glucagon? Thanks

[pi]

Should I know anything about diabetes, insulin and glucagon? Thanks

They're commonly used in questions as scenarios. Usually they'd give you enough information to answer the question, but it's good tact to familiarise yourself with the basics.

I'd be ignoring all the obscure types of diabetes mellitus (MODY, LADA, gestational, etc etc), just have a very brief understanding of type 1 and type 2 imo.

my knowledge of the finer or past-VCE points of Biology is, well, shaky, and until I do the biomed degree I yearn for but will never do, I'll only lead y'all astray

Why is that? Surely your ATAR would get you into a biomed course somewhere (or at the least, a science course where the same stuff can be studied)?

[cosine]

For the question attached, I said the tumour cells will have antigens that will be recognised as self-antigens by the immune cells of the tasmanian devil. Is this correct?

[BakedDwarf]

So does that mean DNA primase adds the primers on DNA during DNA replication?

I'm confused. I thought RNA primase synthesises the primer sequence for DNA replication. What's the difference between DNA and RNA primase?

[Biology24123]

For the question attached, I said the tumour cells will have antigens that will be recognised as self-antigens by the immune cells of the tasmanian devil. Is this correct?

1 mark or 2 mark question. Not sure if you would get the mark as you've basically restated the question. Think you need to say why they are recognised as self

The Tasmanian devil is endangered so the genetic diversity in the species is extremely low meaning all antigens are very similar and are recognised as self

[cosine]

I'm confused. I thought RNA primase synthesises the primer sequence for DNA replication. What's the difference between DNA and RNA primase?

RNA primase synthesises the primer sequence for both the DNA and RNA templates being synthesised. RNA polymerase the synthesises the RNA molecule, whereas DNA polymerase synthesises the DNA molecule.

[cosine]

1 mark or 2 mark question. Not sure if you would get the mark as you've basically restated the question. Think you need to say why they are recognised as self

Just guessing, maybe because it is endangered, the genetic diversity in the species is very low. Or is that too far fetched.

my bad, let me restate:

The tumour cells will have antigens presented on them that are recognised as self-antigens by the immune cells of the devil, and hence no immune response is carried out as they are perceived as own self cells.

2 mark question, unit 3 exam so its not really that related to genetic diversity

[Biology24123]

my bad, let me restate:

The tumour cells will have antigens presented on them that are recognised as self-antigens by the immune cells of the devil, and hence no immune response is carried out as they are perceived as own self cells.

2 mark question, unit 3 exam so its not really that related to genetic diversity

My 2 points would be
- Antigens in all tasmanian devils are very similar (MHC)
- This is due to low genetic diversity within the species

I just googled it and that's what they said

[vox nihili]

For the question attached, I said the tumour cells will have antigens that will be recognised as self-antigens by the immune cells of the tasmanian devil. Is this correct?

No. Remember that self antigens are not recognised at all. The immune system has no capacity to identify self, it can only identify non-self.

RNA primase synthesises the primer sequence for both the DNA and RNA templates being synthesised. RNA polymerase the synthesises the RNA molecule, whereas DNA polymerase synthesises the DNA molecule.

This is not correct. Primase only synthesises RNA primers for DNA replication. RNA polymerases do not need primers.

As an aside: the reason RNA primers are used is because RNA sticks to DNA better than DNA sticks to DNA. Therefore, they don't have a tendency to fall off DNA, as DNA primers would.

[Biology24123]

No. Remember that self antigens are not recognised at all. The immune system has no capacity to identify self, it can only identify non-self.

This is not correct. Primase only synthesises RNA primers for DNA replication. RNA polymerases do not need primers.

As an aside: the reason RNA primers are used is because RNA sticks to DNA better than DNA sticks to DNA. Therefore, they don't have a tendency to fall off DNA, as DNA primers would.

So in the lagging strand, primers are added every so often. What determines when a primer is added, is it when the strand returns to a 5' end?

[cosine]

No. Remember that self antigens are not recognised at all. The immune system has no capacity to identify self, it can only identify non-self.

This is not correct. Primase only synthesises RNA primers for DNA replication. RNA polymerases do not need primers.

As an aside: the reason RNA primers are used is because RNA sticks to DNA better than DNA sticks to DNA. Therefore, they don't have a tendency to fall off DNA, as DNA primers would.

So RNA primase synthesises an RNA Primer in which this attaches to its complementary DNA base. And when this happens, only then is DNA polymerase able to synthesise the new DNA strand?

When we state the steps in DNA replication, do we have to state that RNA primase synthesises RNA primers which bind to the 3' end of the single stranded DNA molecules? Or can we just start by saying that primers are attached to the 3' end and .. ?

[cosine]

The Bacterium U is recognised as non-self as, on its surface, it has:
A. self antigens
B. MHC Class I markers
C. MHC Class II markers
D. glycopeptidase chains

From what I have learnt about the immune system for the past few days, is that only multicellular organisms possess MHC I markers. MHC II markers would be present on APCs and not bacteriums, so B and C are out. I don't know what D even is, so is the answer A? Assuming they are talking about self antigens, that is, self to the bacterium and nonself to the organism that is infected, right?