VCE Biology Question Thread

[Sconey]

Did VCAA ever end up deciding on the total ATP output of aerobic cellular respiration? The atarnotes book says 36-38 (32-34 in ETC) and that's what my teacher said too, but I read in another place that it was 32-34 and another person said 30-32 ... can anyone confirm?

Go with what your teacher and the ATARNotes book says; those figures will be marked correct.

[Sconey]

How are T helper cells involved in the humoral response? apart for APCs presenting antigens to them?

In the humoral response, antigen presenting cells (APCs) present antigens to T helper  (Th) cells in the lymph nodes. This activates the Th cells and produces more activated Th cells. At the same time, a specific B cell able to respond to the pathogen comes into contact with the antigen. The B cell engulfs and displays the antigen and finds an activated Th cell. Once the B cell has presented the antigen to the activated Th cell, the Th cell releases cytokines and activates the B cell to divide and proliferates into plasma cells and Memory B cells. The plasma cells produce specific antibodies for the pathogen, and the Memory B cells remain in the body for future infection.

Hope this helps.

[PhoenixxFire]

Did VCAA ever end up deciding on the total ATP output of aerobic cellular respiration? The atarnotes book says 36-38 (32-34 in ETC) and that's what my teacher said too, but I read in another place that it was 32-34 and another person said 30-32 ... can anyone confirm?

VCAA have said they'll accept either 32 or 34 for ETC and therefore 36 or 38 in total. Don't give a range though.

In the humoral response, antigen presenting cells (APCs) present antigens to T helper  (Th) cells in the lymph nodes. This activates the Th cells and produces more activated Th cells. At the same time, a specific B cell able to respond to the pathogen comes into contact with the antigen. The B cell engulfs and displays the antigen and finds an activated Th cell. Once the B cell has presented the antigen to the activated Th cell, the Th cell releases cytokines and activates the B cell to divide and proliferates into plasma cells and Memory B cells. The plasma cells produce specific antibodies for the pathogen, and the Memory B cells remain in the body for future infection.

Hope this helps.

The Th cell doesn't divide until after it finds the activated B cell (it is stimulated by the cytokines it releases). It's an extra precaution to help prevent autoimmune issues.

[antigony]

Go with what your teacher and the ATARNotes book says; those figures will be marked correct.

Thank you!

VCAA have said they'll accept either 32 or 34 for ETC and therefore 36 or 38 in total. Don't give a range though.

Thanks! I thought the range was supposed to refer to how cellular respiration in prokaryotes produces 2 extra ATP because none is used up to "move" from the mitochondria to the cytoplasm as it is in eukaryotes - is that incorrect?

[PhoenixxFire]

Thank you!

Thanks! I thought the range was supposed to refer to how cellular respiration in prokaryotes produces 2 extra ATP because none is used up to "move" from the mitochondria to the cytoplasm as it is in eukaryotes - is that incorrect?

Nah you're right. VCE way oversimplifies it. There's also some evidence that muscle cells produce more. VCAA does't like ranges though so just pick one.

[pugs]

For the evolution of the genus homo, is this the correct order? (can someone pls confirm whether denisovans or neanderthals are first) also, is it necessary to have memorised the order of homo evolution? :l

Homo habilis
Homo erectus
Homo heidelbergensis
Homo neanderthalensis/Homo denisovan (unsure)
Homo sapiens
Homo floresiensis

also, respiration questions:
- for glycolysis, do we say there is an output of 4 ATP or 2 ATP? (bc of net)
- and is knowledge of pyruvate oxidation necessary?

thanks!!

[DBA-144]

For the evolution of the genus homo, is this the correct order? (can someone pls confirm whether denisovans or neanderthals are first) also, is it necessary to have memorised the order of homo evolution? :l

Homo habilis
Homo erectus
Homo heidelbergensis
Homo neanderthalensis/Homo denisovan (unsure)
Homo sapiens
Homo floresiensis

also, respiration questions:
- for glycolysis, do we say there is an output of 4 ATP or 2 ATP? (bc of net)
- and is knowledge of pyruvate oxidation necessary?

thanks!!

There's actually no order of Human evolution anyways, that is agreed upon. Different theories are presented by different people and thus I don't actually think that there is any accepted order. And its 2 ATP output (net) and no need for oxidation of pyruvates.

Does anyone know what exam score I would need for a 40+ ranked about 3-5th in a weak cohort (0 40+ last year)? Am I correct in saying a 45 is impossible given my rank?

[sandywu]

Hi, I was wondering if someone could explain why the light dependent phase is interdependent with the light independent stage? There was question where the site of light independent stage was inhibited, and it asked whether light dependent stage would proceed. The answer stated that it would not proceed because they were interdependent. Can someone please explain this to me? I thought that light dependent reactions would still occur even if the light independent reaction was inhibited...

[Sconey]

Hi, I was wondering if someone could explain why the light dependent phase is interdependent with the light independent stage? There was question where the site of light independent stage was inhibited, and it asked whether light dependent stage would proceed. The answer stated that it would not proceed because they were interdependent. Can someone please explain this to me? I thought that light dependent reactions would still occur even if the light independent reaction was inhibited...

Interdependent in this case means that the light-dependent reaction requires inputs that the light-independent stage produces as outputs. In this case NADP and ADP + Pi.

[PhoenixxFire]

Does anyone know what exam score I would need for a 40+ ranked about 3-5th in a weak cohort (0 40+ last year)? Am I correct in saying a 45 is impossible given my rank?

Impossible to actually predict it without knowing your cohort specifically - last year around 80% would have gotten you a 40 if you were rank 1. I'd guess that around the 85-90% mark would get you a 40+ with your rank, but it's really impossible to work out without knowing what exam scores your cohort is going to get.
A 45 isn't impossible - hardly anyone gets 100% for bio so getting that or close to it would probably be enough to get you into the high 40s even with lower GA 1 and 2 scores (although dependent on how low). Probably more realistic to expect mid 40s at the highest though.

Hi, I was wondering if someone could explain why the light dependent phase is interdependent with the light independent stage? There was question where the site of light independent stage was inhibited, and it asked whether light dependent stage would proceed. The answer stated that it would not proceed because they were interdependent. Can someone please explain this to me? I thought that light dependent reactions would still occur even if the light independent reaction was inhibited...

Light dependent stage requires an input of NADP+ to attach hydrogen to. This NADPH is then used in the light independent stage and turned back into NADP+. If you're not taking the hydrogens off the NADPH then you won't have any NADP+ to add hydrogens to and the light dependent stage can't happen without those NADP+.

[ssillyssnakes]

Hi, I was wondering if someone could explain why the light dependent phase is interdependent with the light independent stage? There was question where the site of light independent stage was inhibited, and it asked whether light dependent stage would proceed. The answer stated that it would not proceed because they were interdependent. Can someone please explain this to me? I thought that light dependent reactions would still occur even if the light independent reaction was inhibited...

Because some of the inputs of the light dependent stage are NADP+ and ADP+Pi, and these are produced by the light independent stage, the light dependent stage couldn't continue if the light independent stage was inhibited. These molecules wouldnt be present (at least, after a little while), stopping the light dependent stage from occurring.

I'm sure there are more complex processes too that are involved but that's the simplest explanation

[antigony]

Nah you're right. VCE way oversimplifies it. There's also some evidence that muscle cells produce more. VCAA does't like ranges though so just pick one.

Okay, good to know - thank you! As always, VCAA discouraging curiosity ...

[Chocolatemilkshake]

Do leukocytes of the innate immune system (natural killer cells, neutrophils, etc) detect that something is foreign via pattern-recognition receptors? If not, how do they determine the difference between self and non-self? (is it simply because pathogens don't have self markers (MHC I markers) on their surface.

Thanks everyone for answering so many questions 

[IThinkIFailed]

Do leukocytes of the innate immune system (natural killer cells, neutrophils, etc) detect that something is foreign via pattern-recognition receptors? If not, how do they determine the difference between self and non-self? (is it simply because pathogens don't have self markers (MHC I markers) on their surface.

Thanks everyone for answering so many questions 

Not sure about neutrophils,
But my teacher said NK cells essentially just roam around the body trying to bind to “kill” receptors on self cells. If the self cells are normal and not infected by a virus infected or are a cancer cell, then the MHC 1 marker inhibits this signal. However, if they ARE a cancer or virus infected cell, then they will likely have abnormal MHC markers that don’t inhibit the kill signal, as a result, the NK cells degranulate, releasing perforin and granzymes to induce apoptosis in the abnormal self cell.


Now I have a question, can someone see if what I’m saying makes sense?

A substitution mutation where an amino acid changes, would impact the protein formed like this:

It would alter the primary structure of the protein, which in turn could affect the tertiary structure as it may alter bonds that form the protein’s specific 3D shape. As a result, a different tertiary structure resulrs, which may not be specific to the function of the protein, inhbiiting it from being able to perform its function.

[Livcur16]

Hey,
Just wondering, if all our cells have the same suite of antigens, then why do autoimmune diseases only affect certain types of cells?

Also, on second exposure to a pathogen, do the memory Th cells have to still activate the memory B cells and memory Tc cells, or is there another path that occurs?
Thankyou