VCE Biology Question Thread

[1292]

Hello,
Does anyone have any advice on what to do in the coming days leading up to the exam? I have done all the past papers I have access to and I'm feeling a little at loss with what to do now... Thanks in advance!

[Erutepa]

Hello,
Does anyone have any advice on what to do in the coming days leading up to the exam? I have done all the past papers I have access to and I'm feeling a little at loss with what to do now... Thanks in advance!

1. Make sure you've harshly marked you're past exams, or got a teacher to do it. You're not going to gain anything from going easy on yourself.
2. Make sure you've gone through all the exams you've done and understand what you got wrong and how you got it wrong. If there's weaker areas in you're knowledge that you keep getting questions wrong about, you might want to make some summary notes or draw a diagram or something else that helps you revise that content.
3. I would then make sure you actually redo any questions you've got wrong. It's easy to read the answer sheet and tell yourself that you'll remember the correct response for next time, but I think it's far better to be rewriting and questions answered incorrectly.
4.do more practices exams. You may have done all the past vcaa ones, but I'm sure you're teacher has company exams that you could ask for.

Hope this helps, and good luck with biology.

[Evolio]

You need to talk about a type of reproductive isolation (they are in the same location at the same time so that's the type of isolation that must be occuring).

I don't understand this part. Could you please clarify? What do you suggest when answering this question? I still don't understand why competition wouldn't be a reason for interbreeding not to occur.

[Rom_Dog]

I don't understand this part. Could you please clarify? What do you suggest when answering this question? I still don't understand why competition wouldn't be a reason for interbreeding not to occur.

With reproductive isolation the individuals cannot naturally mate. This may be behavioural, for example they are too phenotypically different so refuse to mate with each other or it may be physically impossible because genitalia might not be compatible which is the case for many species of flys. Even though they can't naturally produce offspring, through human intervention this may be possible. 

I hope this answers part of your question!

[Bri MT]

I don't understand this part. Could you please clarify? What do you suggest when answering this question? I still don't understand why competition wouldn't be a reason for interbreeding not to occur.

You're thinking on an individual level whereas you should be thinking on a subpopulation level.

Competition for resources would not result in two subpopulations becoming distinct,  it would result in traits giving a competitive advantage becoming more common in subsequent generations (assuming a bunch of conditions are met)

 In just about every population the number of organisms which produce fertile offspring in each generation is less than the number of organisms in that generation (remember competition to survive & reproduce as a component  of evolution by natural selection?). If you have a population that's changing allele frequencies that's evolution but this does not mean that speciation is occurring.

For speciation you need to have groups that are having their allele frequencies become more different over generations.  Thus, you need some sort of barrier to gene flow between the groups so they don't keep making each other more similar. Competition might prevent some individuals from breeding but it doesn't prevent populations from breeding.

[IThinkIFailed]

Why do allergic responses get worse upon second and third exposures?

I wrote that it is because of pre existing memory cells from the first response, which induces a greater and faster response upon which more Ig E antibodies are produced and prime mast cells by binding to their surface receptors, such that upon reexposure more mast cells are activated via crosslinkage with the allergen and more histamine is released, causing heightened inflammation.

I find it a weird answer though, because it doesn’t really mention why it’s worse upon the second exposure, and it’s moreso about the third and future exposures to the allergen. Can someone check over it?

[BitcoinEagle]

Why do allergic responses get worse upon second and third exposures?

I wrote that it is because of pre existing memory cells from the first response, which induces a greater and faster response upon which more Ig E antibodies are produced and prime mast cells by binding to their surface receptors, such that upon reexposure more mast cells are activated via crosslinkage with the allergen and more histamine is released, causing heightened inflammation.

I find it a weird answer though, because it doesn’t really mention why it’s worse upon the second exposure, and it’s moreso about the third and future exposures to the allergen. Can someone check over it?

This is a pretty good answer. The reason that second and third responses are successively more extreme, is simply because, in each successive response, more antibodies are created which bind to more mast cells. Hence, when the body is reexposed to the antigen, each successive time, more histamine is released and hence the inflammation symptoms including constriction of airways, reddening and swelling etc increase. This can be dangerous if the levels of histamine are high enough.

To everyone else:
In STAV 2018, Q5:

Transcription in:
a) Eukaryotic cells differ from that in prokaryotic cells as eukaryotic cells do not have promoters like eukaryotic cells.
b)Eukaryotic cells differ from that in prokaryotic cells as eukaryotic cells require transcription factors to bind to a promoter region whereas prokaryote cells do not
C) Both eukaryotic cells and prokaryotic cells occur in the cytosol of the cell.
D) Both eukaryotic and prokaryotic cells involve modification of the transcribed RNA.

How is the correct answer discerned here?
 

[darkz]

Transcription in:
a) Eukaryotic cells differ from that in prokaryotic cells as eukaryotic cells do not have promoters like prokaryotic cells.
b)Eukaryotic cells differ from that in prokaryotic cells as eukaryotic cells require transcription factors to bind to a promoter region whereas prokaryote cells do not
C) Both eukaryotic cells and prokaryotic cells occur in the cytosol of the cell.
D) Both eukaryotic and prokaryotic cells involve modification of the transcribed RNA.

A: Eukaryotes have promoters
C: Transcription occurs in the nucleus for Eukaryotic
D: Prokaryotes don't have post-transcriptional factors

That leaves B.

[pugs]

this is a reallyy simple question but the answer to this question in a prac exam is tripping me up so i'm wondering if someone can please clarify it for me

i'm pretty sure that channel proteins are involved in facilitated diffusion only, right?

[caffinatedloz]

this is a reallyy simple question but the answer to this question in a prac exam is tripping me up so i'm wondering if someone can please clarify it for me

i'm pretty sure that channel proteins are involved in facilitated diffusion only, right?

Protein channels are involved in facilitated diffusion, but I'm 99% sure that they're also involved in active transport.

[BitcoinEagle]

this is a reallyy simple question but the answer to this question in a prac exam is tripping me up so i'm wondering if someone can please clarify it for me

i'm pretty sure that channel proteins are involved in facilitated diffusion only, right?

Correct! Channel proteins can be used only in facilitated diffusion as molecules move through it down its concentration gradient without ATP Input.
I believe it would be carrier proteins (which are a little bit different) which can be used for both active and passive transport. Clarification would be great on this point though.

[PhoenixxFire]

this is a reallyy simple question but the answer to this question in a prac exam is tripping me up so i'm wondering if someone can please clarify it for me

i'm pretty sure that channel proteins are involved in facilitated diffusion only, right?

It's more complicated than you're taught in VCE. For the exam, just assume that channel proteins are only for facilitated diffusion, and that carrier proteins can be used for both - but if you get a question about active transport, talk about carriers not channels.

[IThinkIFailed]

This is a pretty good answer. The reason that second and third responses are successively more extreme, is simply because, in each successive response, more antibodies are created which bind to more mast cells. Hence, when the body is reexposed to the antigen, each successive time, more histamine is released and hence the inflammation symptoms including constriction of airways, reddening and swelling etc increase. This can be dangerous if the levels of histamine are high enough.

To everyone else:
In STAV 2018, Q5:

Transcription in:
a) Eukaryotic cells differ from that in prokaryotic cells as eukaryotic cells do not have promoters like eukaryotic cells.
b)Eukaryotic cells differ from that in prokaryotic cells as eukaryotic cells require transcription factors to bind to a promoter region whereas prokaryote cells do not
C) Both eukaryotic cells and prokaryotic cells occur in the cytosol of the cell.
D) Both eukaryotic and prokaryotic cells involve modification of the transcribed RNA.

How is the correct answer discerned here?
 

Thanks for the help!

Now, I have another question:

Is tertiary structure synonymous with 3D shape of a protein?

Also, does this response make sense when explaining the impact of a very high temperature above optimum on enzyme reaction rate?

With high temperatures above optimum, the enzymes bonds denature, leading to a conformational change in the 3D shape of the enzyme, changing its active site shape and reducing the ability of the substrate to bind to the active site, reducing the rate of reaction.

I’m not sure if I need to specific what type of bonds e.g is it hydrogen bonds, or disulphides bonds, and I also feel it can be more concise but i can’t seem to discern which details to remove.

[caffinatedloz]

It's more complicated than you're taught in VCE. For the exam, just assume that channel proteins are only for facilitated diffusion, and that carrier proteins can be used for both - but if you get a question about active transport, talk about carriers not channels.

Thank you very much!!

[xxxjss]

Thanks for the help!

Now, I have another question:

Is tertiary structure synonymous with 3D shape of a protein?

Also, does this response make sense when explaining the impact of a very high temperature above optimum on enzyme reaction rate?

With high temperatures above optimum, the enzymes bonds denature, leading to a conformational change in the 3D shape of the enzyme, changing its active site shape and reducing the ability of the substrate to bind to the active site, reducing the rate of reaction.

I’m not sure if I need to specific what type of bonds e.g is it hydrogen bonds, or disulphides bonds, and I also feel it can be more concise but i can’t seem to discern which details to remove.

I'd say that the tertiary structure is the overall three dimensional shape of the protein, as technically alpha helices and beta pleated sheets are 3D too; tertiary is the folding of these structures spatially through the bonding between the variable R groups (side chains).

 I think you can get away with not mentioning the specific bonds, although if your worried you can just chuck hydrogen bonds in brackets
This is how i describe high temperature's effect on enzyme activity:
As the temperature exceeds the enzyme's optimal, bonds are broken in it's tertiary/secondary structure, distorting the structure of the active site to the extent where it will no longer be able to bind to the substrate, thereby reducing the rate and ability to catalyse. Basically the same length as yours!