VCE Biology Questions Thread

md2112

ok thanks do we need to know about the dates when the new homminn species diverged

atarwonders

hi i need help with 4 a. sample exam

Christ

atarwonders
So with question 4a,
As the Indigenous population and the British population had never come in contact, Aboriginal's did not have the adaptive immunity in terms of B memory cells against the pathogens carried by the British, including smallpox, which resulted in deadly infection in the Aboriginals.
I believe to get the third mark you have to mention how British people had active immunity against smallpox and hence able to fight off infection and so the severity of infection was not as bad as in the aboriginal population

Pasta

md2112 It is Denisovans. There is 4-6% similarity in the nuclear DNA shared amongst Indigenous Australians, Papua New Guineans and Indonesians and this covers the likely route to Australia (as seen in the article). Homo erectus and Home floresiensis were in the areas near Sahul at the time of the migration to Australia but none of their nuclear DNA is shared with indigenous Australians.
(It’s not H. erectus because the article states clearly that no other species apart from Denisovans shared nuclear DNA with Indigenius Australians).

md2112

Pasta and so why isn't it floresis

chemistry1111

for question 6 multiple choice of the vcaa 2019 exam,
why is the answer D and not B. Thank you

_sophiestudies_

chemistry1111 it cannot be B because the question has stated that aldicarb is a reversible inhibitor of acetylcholinesterase. This means it will form weak intermolecular bonds with the the enzyme (not strong covalent bonds like irreversible inhibitors), allowing it to detach from the active site (reversible = non-permanent). B says it strongly binds to the active site of acetylcholinesterase, which is therefore incorrect. A is also incorrect because the question already states that it is reversible, not permanent/irreversible. C is incorrect because inhibitors prevent the substrate from being catalysed by the enzyme, meaning the rate of the breakdown of acetylcholine cannot increase. D is correct because it will reduce the activity of acetylcholinesterase, binding to its active site and "reducing the number of active sites for acetylcholine to bind to". Hope that helps!

Smartiestarz

md2112 It’s not H floresiensis because they tend to have smaller stature so compared to Aboriginal Australians who are much larger, they couldn’t be the ancestor - you can also probably talk in terms of cranial capacity and how it was found much more recently than 50000/60000 years ago when Aboriginal Australians first arrived into Sahul. The only confusion comes with H Denisova and H erectus
Because it says “fossils from this time period include H erectus” I’d argue that H erectus lived in the same time period as the aboriginal Australians so its not likely to be an ancestor (also considering the lack of similarity of nuclear DNA)
I feel like although H denisova only shares 4-6% nuclear DNA in common its probably the best answer here accoridng to the information given in the passage

studyingvce2022

do i need to know the specific amounts of products/inputs for cellular respiration and photosynthesis?

md2112

studyingvce2022 no you just need to know the specific atp

chemistry1111

has the master gene been removed from course

md2112

Smartiestarz ok, also how do cytotoxic t cells get activated by t helper cell

md2112

what are two differences between cytotoxic t cells and natural killer cells

Smartiestarz

md2112

Cytotoxic T cells are involved in an adaptive immune response (cell mediated) and they release chemicals like perforins to induce apoptosis in virally infected cells upon binding to the non self antigen presented on MHC 1 markers of the infected host cell
Whereas natural killer cells are involved in the innate immune response. It detects the lack of MHC 1 markers on a host cell and recognises it as “non self” releasing granzymes initiating a death ligand that causes apoptosis

_sophiestudies_

md2112 cytotoxic t cells are part of the adaptive cell-mediated response, whereas natural-killer cells are non-specific immune cells part of the innate immune system (second line of defence). Cytotoxic t cells will therefore specifically bind to MHC I markers/antigens it's initial T cell was selected for, whereas natural killer cells will target any foreign MHC I markers it notices on viral infected cells or tumour cells. Also, natural killer cells have killer activation and killer inhibition receptors that indicate whether it kills the cell, whereas cytotoxic t cells are already programmed to kill the cell that they bind to using their t cell receptor.

md2112

Smartiestarz ok thanks, also do u know how do cytotoxic t cells get activated by t helper cell

Smartiestarz

Also can someone please explain the Q9 C ii) of the 2022 sample exam on mtDNA phylogeny - I kind of get it but not fully- espcially the part about “continuous presence” of aboriginal Australian populations

Smartiestarz

Smartiestarz ^^

_sophiestudies_

md2112 Cytotoxic T cells produced from the expansion and differentiation of the selected T cell are activated by Helper T cells via the release of cytokines, as well as through binding to the first MHC I marker it finds on an infected cell. Both allow it to be activated.

md2112

_sophiestudies_ thank you so much

md2112

guys im confused with the question 1c on the sample exam, it says will the "enzymes for tryptophan sysntehis be produced", can someone please help

_sophiestudies_

md2112 the structural genes in the trp operon each code for separate enzymes that are involved in the formation of tryptophan. Here are the details (don't need to know this though):

TrpE and TrpD -> Form enzyme Anthranilate synthase, which converts chorismate (found in the cell) into anthranilate.
TrpC -> Forms enzyme Indole-3-glycerol-photosphate synthase, which converts anthranilate into indole-3-glycerol-photosphate.
TrpB and TrpA -> Forms enzyme Tryptophan synthase, which converts indole-3-glycerol-photosphate into tryptophan.
(Requires lots of energy, meaning the process needs to be tightly regulated via attenuation and repression mechanisms).

Here in the structure of the trp operon to help as well (would ensure you know this):

3' end - Promoter - Operator - Leader (TrpL) - Attenuator - TrpE - TrpD - TrpC - TrpB - TrpA - Trailer - 5' end

Hopefully this will help you understand the question!

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