VCE Biology Question Thread

[PhoenixxFire]

Just wondering in regards to the Kreb Cycle if we should say that the pyruvate molecule or acetyl coenzyme A is used as an input?

Thanks heaps!

You should be fine with using either. Technically the input is acetyl co-A but a lot of people won't be taught that because the details of krebs have been removed from the study design.

I've had a quick look through past examiners reports:
2016: Pyruvate is referred to as a substrate of the kreb's cycle
2010: "• Krebs (cycle): pyruvate is converted to carbon dioxide, 2 ATP produced "
2017: "The structure labelled Y is where: D. pyruvate is broken down, releasing carbon dioxide"

I only found one reference to acetyl coA and it was talking about details that are no longer on the study design. So I would just go with pyruvate but you should be fine to use either.

[PopcornTime]

Can I include anything else in the following response that VCAA would want?

Humoral response
Overall: involves B cells and results in the production of specific antibodies that act against pathogens

Steps:
- dendritic cells destroy invading pathogen and present pathogen’s antigen on their surface
- B cell binds with specific antigen and is activated by T-helper cell
- B cell divides into plasma cells and memory cells
- plasma cell produces and secretes antibody molecules
- formation of antigen-antibody complex and promotion of phagocytosis
- memory B cell remains in circulation, ready to respond to same antigen if encountered again

[PhoenixxFire]

Can I include anything else in the following response that VCAA would want?

Humoral response
Overall: involves B cells and results in the production of specific antibodies that act against pathogens

Steps:
- dendritic cells or macrophages destroy invading pathogen and present pathogen’s antigen on MHC 2 markers ontheir surface
-T-Helper cell binds to the antigen presented on the MHC2 and is activated
- B cell binds with specific antigen and is activated(It is sort of already activated) Stimulated to divides and differentiate by T-helper cell You need to link this to the MHC2 (I've added a step but you can put it on the end of the first step if you want)
- B cell divides and differentiates into plasma cells and memory cells
- plasma cell produces and secretes antibodiesy molecules
- formation of antigen-antibody complex and promotion of phagocytosis
-You need to include something about removing extracellular pathogens to show that you know it is extracellular immunity.
- memory B cell remains in circulation, ready to respond to same antigenantigen with same specificity if encountered again

[vox nihili]

Well as Vox said, because the actual quantity of glucose produced is rather small over the 140 seconds in comparison with the total glucose available in the cell - probably only around 1%, thus there just wasn’t enough time to show the plant consuming the freshly stored glucose - and probably just used existing starch granules

This is a really good explanation!

[darkz]

This is a really good explanation!

I agree 

[PopcornTime]

The following is the dot point on the lymphatic system in the study design:

"The role of the lymphatic system in the immune response including the role of secondary lymphoid tissue (with reference to lymph nodes) as the site of antigen recognition by lymphocytes, and as a transport system for antigen presenting cells including dendritic cells."

What exactly should we know about the lymphatic system in relation to the immunity topic (what is relevant to the exam) and how much detail should we know?

[Poet]

Hey all,
Could someone please give me the definition of an acceptor molecule in layman's terms?
Are they different to carrier molecules?
Thank you!!

[darkz]

Hey all,
Could someone please give me the definition of an acceptor molecule in layman's terms?
Are they different to carrier molecules?
Thank you!!

Acceptor molecules are basically those which accept/receive other particles such as protons (hydrogen ions), electrons etcetera. I suppose you could say that they are technically "carrier molecules" for example, NADP+ accepts electrons and protons to form NADPH and is hence a carrier molecule. And the final electron acceptor in the electron transport chain in respiration is Oxygen, which combines with the electrons and hydrogen ions to form water - which I suppose you could call a carrier molecule, as it provides the electrons/protons needed in the light dependent reactions in photosynthesis

[Poet]

Acceptor molecules are basically those which accept/receive other particles such as protons (hydrogen ions), electrons etcetera. I suppose you could say that they are technically "carrier molecules" for example, NADP+ accepts electrons and protons to form NADPH and is hence a carrier molecule. And the final electron acceptor in the electron transport chain in respiration is Oxygen, which combines with the electrons and hydrogen ions to form water - which I suppose you could call a carrier molecule, as it provides the electrons/protons needed in the light dependent reactions in photosynthesis

Okay, thank you so much! That makes sense now. <3
So, would you then say that FADH₂ is or isn't an acceptor molecule?

[PhoenixxFire]

I've never learnt much about the difference (or lack of) between them but I would just stick with carrier molecule because that is what VCAA uses in the study design.

[darkz]

Okay, thank you so much! That makes sense now. <3
So, would you then say that FADH₂ is or isn't an acceptor molecule?

FADH2 would not be an acceptor molecule as it is already it its loaded form so it acts as a donator, instead of acceptor. FAD would be an acceptor as it accepts electrons/protons to form FADH2

Edit: typo

[peachxmh]

When a hydrophilic signalling molecule binds to a receptor on a cell, why does this cause the intracellular part of the receptor to change shape and activate molecules (e.g. second messengers, G proteins) inside the cell? Thanks

[TheBigC]

When a hydrophilic signalling molecule binds to a receptor on a cell, why does this cause the intracellular part of the receptor to change shape and activate molecules (e.g. second messengers, G proteins) inside the cell? Thanks

Very interesting question!

The "why" questions are often quite ambiguous pertaining to the amount of depth expected, though what I can intimate is that hydrophilic signalling molecules each contain various regions of charge, polarity or non-polarity etc. and it is these factors that - upon binding to the receptor - interact with accompanying charges (etc) at the site of ligation and ultimately cause a change in shape of the receptor (this is analogous to the method by which a protein confronts a change in shape during denaturation consequentially to encountering specific environmental factors). This change in shape, furthermore, alters the interactions between this receptor and substances within cells, thence triggering the characteristic signal transduction cascade.

[peachxmh]

Very interesting question!

The "why" questions are often quite ambiguous pertaining to the amount of depth expected, though what I can intimate is that hydrophilic signalling molecules each contain various regions of charge, polarity or non-polarity etc. and it is these factors that - upon binding to the receptor - interact with accompanying charges (etc) at the site of ligation and ultimately cause a change in shape of the receptor (this is analogous to the method by which a protein confronts a change in shape during denaturation consequentially to encountering specific environmental factors). This change in shape, furthermore, alters the interactions between this receptor and substances within cells, thence triggering the characteristic signal transduction cascade.

I must say a huge thank you for this explanation! It's really made things much clearer

[PopcornTime]

If an enzyme has an optimum temp of 38ºC, then what does this suggest about efficiency and collisions? I assume its maximum efficiency, but are there any other key terms/phrases?