VCE Biology Question Thread

[plsbegentle]

yeah buddy, had the STAV 2016 one, didn't worry about studying for it too much  but got 93% so pretty pleased, was of decent difficulty, hbu? (cohort average was really low but, like 60%)

yeh haha i did mine yesterday, totally stuffed up the cox 1 and 2 enzyme question other than that it was pretty easy

[vox nihili]

sorry to double post but also
Why is it advantageous for multiple different types of proteins to be involved in dna replication? This is practice sac question and it is really confusing

Probably a bit rough for a VCE biol SAC to be honest. Major reason is that the more proteins you have, the more control you can exert over DNA replication. It means that you have to have all the pieces in place before it will replicate, meaning that you can decide when and under what conditions those pieces are in place (i.e. when to start replication).

[The Usual Student]

Probably a bit rough for a VCE biol SAC to be honest. Major reason is that the more proteins you have, the more control you can exert over DNA replication. It means that you have to have all the pieces in place before it will replicate, meaning that you can decide when and under what conditions those pieces are in place (i.e. when to start replication).

Mr T Rav you are an absolute GUN!!!!
Thanks man!
Final question before my sac tomorrow hahaha
Why does DNA have to be condensed before replication? why do they need to be condensed into chromosomes?
Is it more efficient?
Also, why are thye split into several chromosomes and not just like one huge one?
Thanks !!

[TheAspiringDoc]

Mr T Rav you are an absolute GUN!!!!
Thanks man!
Final question before my sac tomorrow hahaha
Why does DNA have to be condensed before replication? why do they need to be condensed into chromosomes?
Is it more efficient?
Also, why are thye split into several chromosomes and not just like one huge one?
Thanks !!

I think it's neater (like easier to part them at the centromere) when they condense, and if there are multiple chromosomes rather than one, then that allows for greater variation as a result of meiosis

[The Usual Student]

I think it's neater (like easier to part them at the centromere) when they condense, and if there are multiple chromosomes rather than one, then that allows for greater variation as a result of meiosis

thanks!
I was thinking that but what about for mitosis? The question was refering to mitosis and not meiosis
Yeah it is a weird question and it had stumped all my friends

[vox nihili]

Mr T Rav you are an absolute GUN!!!!
Thanks man!
Final question before my sac tomorrow hahaha
Why does DNA have to be condensed before replication? why do they need to be condensed into chromosomes?
Is it more efficient?
Also, why are thye split into several chromosomes and not just like one huge one?
Thanks !!

I think it's neater (like easier to part them at the centromere) when they condense, and if there are multiple chromosomes rather than one, then that allows for greater variation as a result of meiosis

You wouldn't be expected to know why the condensation is relevant. I suspect TheAspiringDoc's answer is probably what they're looking for though. It allows them to be dragged around properly.

Condensation of DNA is actually really important for controlling gene expression though, but yeah, that's like second or third year uni stuff, not VCE Biol...

[The Usual Student]

You wouldn't be expected to know why the condensation is relevant. I suspect TheAspiringDoc's answer is probably what they're looking for though. It allows them to be dragged around properly.

Condensation of DNA is actually really important for controlling gene expression though, but yeah, that's like second or third year uni stuff, not VCE Biol...

thanks!
They probably wont have much of that on the sac then! Phew

[Butterflygirl]

Hey guys, I have some questions for vce bio 3/4:

Do I need to know the definition/function of every organelle? What other definitions are essential to know?

For the question that follows, is my answer correct?: What are two functions of interferon in terms of virus infected cells?
Interferon increases the resistance of nearby cells from viral infection. Also, since interferon is released from a virus infected cell, it signals cytotoxic T cells which then release chemicals that lyse the virus infected cell and induce cell death.

Thankyou so much >.<

[vox nihili]

Hey guys, I have some questions for vce bio 3/4:

Do I need to know the definition/function of every organelle? What other definitions are essential to know?

For the question that follows, is my answer correct?: What are two functions of interferon in terms of virus infected cells?
Interferon increases the resistance of nearby cells from viral infection. Also, since interferon is released from a virus infected cell, it signals cytotoxic T cells which then release chemicals that lyse the virus infected cell and induce cell death.

Thankyou so much >.<

Yes, you do need to know what each organelle does.

Yep, that's pretty much interferon in a nutshell

[blacksanta62]

Hey, I'm currently reading chapter 9 from the 'NOB' and can't seem to answer this question:
"what type of genotype is necessary for a recessive trait to be expressed for an autosomal gene?"

Can someone explain this please?
Thank you

[vox nihili]

Hey, I'm currently reading chapter 9 from the 'NOB' and can't seem to answer this question:
"what type of genotype is necessary for a recessive trait to be expressed for an autosomal gene?"

Can someone explain this please?
Thank you

Weirdly phrased. I think it's just looking for homozygous.

[blacksanta62]

Weirdly phrased. I think it's just looking for homozygous.

Hey T-Rav, I'm still a bit confused on why it's homozygous. Why can't it be hetrozygous? I'm struggling a bit with this topic so I may start asking a lot more questions

[TheAspiringDoc]

Hey T-Rav, I'm still a bit confused on why it's homozygous. Why can't it be hetrozygous? I'm struggling a bit with this topic so I may start asking a lot more questions

Recessive alleles only are phenotypically expressed if there is no dominant allele to "mask" them. Now, the reason NoB has specified that the recessive allele is autosomal (non sex-linked [i.e. Not X-linked or Y-linked]) is that if it is allosomal (I.e. Sex-linked), then in a male, there is only one X chromosome and hence it is not possible in a male for dominance between alleles on sex chromosomes (unless in the very unlikely case that the allele is also on the Y-chromosome). So if it's X-linked it doesn't work. If it's Y-linked, there there also isnt really any recessive/dominant interaction as males only have one Y-chromosome.
Now that that is out of the way..

Homozygous = Two identical alleles for particular gene (one on each homologous chromosome)
Heterozygous = Two different alleles for a particular gene (one on each homologous chromosome)

Btw, a dominant allele "masks" a recessive allele if an individual has both types of allele (which makes them heterozygous).

So if you logically connect the dots, does it make sense that for a person who has two loci for a given gene, if they have a recessive phenotype they must be homozygous (because if they had two different alleles, one would likely be dominant over the other)

Yeah hopefully that makes sense and sorry I'm so inconcise

[gameboy99]

This my note on Inflammation including most of the mechanisms of the second line of defence except for interferon and NK cells.
Please correct mistakes in this because I am certain there is a few mistakes here and there. 

1. APC cells such as macrophages and dendritic cells bind to receptors of damaged cells and release cytokines. (not sure with that sentence) In addition to this, mast cells, basophils and platelets all release histamine. All of this together stimulate nearby blood vessels to dilate and become more permeable allowing for more blood flow to the localized area.
2. Neutrophils and monocytes come with blood and get out of bloodstream and go into the extracellular fluid.
3. Complement proteins also come from the bloodstream which perforate the cell wall of the pathogen making it easier for phagocytosis to occur.
4. After macrophages ingest pathogen, it releases interleukin 1 into the blood stream which sends message to hypothalamus to increase body temperature reducing the growth of the pathogen.
5. Pus may form from phagocytes eventually dieing
6. Blood clotting has occurred
*Simultaneously, the 3rd line of defence is occuring with B cells making antibodies, however they may not be used if the pathogen is killed quickly

[vox nihili]

This my note on Inflammation including most of the mechanisms of the second line of defence except for interferon and NK cells.
Please correct mistakes in this because I am certain there is a few mistakes here and there. 

1. APC cells such as macrophages and dendritic cells bind to receptors of damaged cells and release cytokines. (not sure with that sentence) In addition to this, mast cells, basophils and platelets all release histamine. All of this together stimulate nearby blood vessels to dilate and become more permeable allowing for more blood flow to the localized area.
2. Neutrophils and monocytes come with blood and get out of bloodstream and go into the extracellular fluid.
3. Complement proteins also come from the bloodstream which perforate the cell wall of the pathogen making it easier for phagocytosis to occur.
4. After macrophages ingest pathogen, it releases interleukin 1 into the blood stream which sends message to hypothalamus to increase body temperature reducing the growth of the pathogen.
5. Pus may form from phagocytes eventually dieing
6. Blood clotting has occurred
*Simultaneously, the 3rd line of defence is occuring with B cells making antibodies, however they may not be used if the pathogen is killed quickly

1. They don't necessarily bind receptors on damaged cells. They tend to bind chunks of damaged cells or mediators that those cells release to tell everyone they're damage. Also, they can also bind to antigens (inflammation occurs in infection too!).
2. (Y)
3. Perforation doesn't make it easier to phagocytose. It kills the bacterium. Making the pathogen easier to phagocytose is an additional role of complement, unrelated to killing.
4. Don't specify IL-1. TNF, IL-6 and interferons all do this too—you're better just to say cytokine.
5. (Y) mainly neutrophils
6. (Y)
* I'd drop the part about not being used


Immunology is an absolute minefield; this was a very good example of someone navigating it really well.