Psyxwar's Biology 3/4 Question Thread

[psyxwar]

Oddly enough, it's true. Like any other chemical reaction, the ETC has its clear inputs and outputs. Due to the Laws of Conservation (e.g. energy, mass etc), it would be chemically impossible - under current understanding, anyway - for the electron transport chain to produce 33 units of ATP. Due to the ETC's reactants, only 32 or 34 units can be produced, not anything in-between.

There are three reasons we cannot state an exact number of ATP molecules generated by the breakdown of one molecule of glucose.
First, phosphorylation and the redox reactions are not directly coupled to each other, so the ratio of the number of NADH molecules to the number of ATP molecules is not a whole number. We know that 1 NADH results in 10 H* being transported out across the inner mitochondrial membrane, but the exact number of H* that must reenter the mitochondrial matrix via ATP synthase to generate 1 ATP has long been debated.

Based on experimental data, however, most biochemists now agree that the most accurate number is 4 H*. Therefore, a single molecule of NADH generates enough proton-motive force for the synthesis of 2.5 ATP. The citric acid cycle also supplies electrons to the electron transport chain via FADH2, but since its electrons enter later in the chain, each molecule of this electron carrier is responsible for transport of only enough H* for the synthesis of 1.5 ATP. These numbers also take into account the slight energetic cost of moving the ATP formed in the mitochondrion out into the cytosol, where it will be used.

Second, the ATP yield varies slightly depending on the type of shuttle used to transport electrons from the cytosol into the mitochondrion. The mitochondrial inner membrane is impermeable to NADH, so NADH in the cytosol is segregated from the machinery of oxidative phosphorylation. The 2 electrons of NADH captured in glycolysis must be conveyed into the mitochondrion by one of several electron shuttle systems. Depending on the kind of shuttle in a particular cell type, the electrons are passed either to NAD* or to FAD in the mitochondrial matrix (see Figure 9.16). If the electrons are passed to FAD, as in brain cells, only about 1.5 ATP can result from each NADH that was originally generated in the cytosol. If the electrons are passed to mitochondrial NAD*, as in liver cells and heart cells, the yield is about 2.5 ATP per NADH.

A third variable that reduces the yield of ATP is the use of the proton-motive force generated by the redox reactions of respiration to drive other kinds of work. For example, the proton-motive force powers the mitochondrion s uptake of pyruvate from the cytosol. However, if all the proton-motive force generated by the electron transport chain were used to drive ATP synthesis, one glucose molecule could generate a maximum of 28 ATP produced by oxidative phosphorylation plus 4 ATP (net) from substrate-level phosphorylation to give a total yield of about 32 ATP (or only about 30 ATP if the less efficient shuttle were functioning)

Above is from Campbell's Biology.

tl;dr: can't energy be lost in the operation of ATP synthase (ie. not all the proton-motive force generated is necessarily harvested)?

[vox nihili]

I looked through a first year text and the 32-34 ATP output is wrong in itself. The amount isn't concrete and varies due to a lot of factors apparently, and it certainly isn't a 32 or 34 scenario. But even in the context of 3/4 bio I've never seen something like this (where they flat out say it's not a range between 32-34, but just 32 OR 34) before.

Like Alon eluded too, our understanding of it isn't concrete. In reality, the yields often go down into the 20s due to leaky membranes and so forth.

[psyxwar]

Yeah, fair enough. What I'm saying is that the number doesn't seem to be concrete as suggested by the exam paper I was doing.

Viruses can be targeted to specific marker molecules on different cell types. With this knowledge, what type of cell in the body would the MAA inducing retrovirus infect?

MAA = autoimmune disease where muscles in arms and legs are broken down (attacked by T cells).

The answers say that they'd infect T-cells, but how would infecting T-cells cause them to attack self cells? I went with muscle cells because I thought infected muscle cells -> displaying antigenic fragments on MHCI -> T cells kill them, leading to an autoimmune-esque scenario?

[vox nihili]

Yeah, fair enough. What I'm saying is that the number doesn't seem to be concrete as suggested by the exam paper I was doing.

Viruses can be targeted to specific marker molecules on different cell types. With this knowledge, what type of cell in the body would the MAA inducing retrovirus infect?

MAA = autoimmune disease where muscles in arms and legs are broken down (attacked by T cells).

The answers say that they'd infect T-cells, but how would infecting T-cells cause them to attack self cells? I went with muscle cells because I thought infected muscle cells -> displaying antigenic fragments on MHCI -> T cells kill them, leading to an autoimmune-esque scenario?

Hmm I agree with you on this one. No doubt there is a way, but it's an extremely poorly worded question and not one that could be reliably answered without a much more advanced knowledge of immunology. Something a VCE student, nor I, would have.

[psyxwar]

Yeah, fair enough.

Do I need to specify the use of a placebo even when we're dealing with non-humans (for experimental design)? eg. giving some mice with HD a drug, and the others a placebo

[Yacoubb]

Yeah, fair enough.

Do I need to specify the use of a placebo even when we're dealing with non-humans (for experimental design)? eg. giving some mice with HD a drug, and the others a placebo

It's probably best to state that while the experimental group is given a particular drug, the control group is given a placebo, ultimately to be able to observe the effects of a drug, and conparing this to the control group.

It also makes you look a bit schmancy fancy!

[simpak]

Hmm I agree with you on this one. No doubt there is a way, but it's an extremely poorly worded question and not one that could be reliably answered without a much more advanced knowledge of immunology. Something a VCE student, nor I, would have.

I think a problem with this question is that it says autoimmune disease and strictly speaking if a virus infects the tissues and the T cell attacks that tissue that is not an autoimmune disease because the T cell is not reacting against a self antigen.  This is just like when a T cell kills any
other tissue infected with any other virus and we call that a response to infection rather than an autoimmune disease.

I think if they asked you this q on a paper there would be outrage.

READ ON FOR INTERESTS SAKE ONLY...
I'm not really sure of like, the 'right answer' but considering it's a retrovirus possible reasons could include: it integrates its genome into the T cell it infects, causing the T cell to become activated and/or proliferate and this T cell happens to be reactive towards a self antigen expressed on the muscle.  Alternatively, if the virus infects and kills CD4 cells like HIV you could have a loss of Tregs that would normally control self-reactive cells and prevent them from responding to the muscle antigens and once these cells are removed CD8 cells could start killing the muscle tissue.
There is a high incidence of autoimmunity in HIV patients even with HAART treatment (combination drug therapy) and HIV is a retrovirus, so apparently they might be trying to force the student to make some kind of link.
I think the key is that if the muscle tissue itself is expressing antigens of the virus that is NOT autoimmunity in a classical sense - autoimmunity occurs when cells are responding against self antigens specifically.  An autoimmune response can be triggered by a microbe but typically there would be either a cross-reacting antibody (ie antibody against microbe also binds self tissues) or the microbe provides maturation signals to a dendritic cell that allows the dendritic cell to express a self antigen to T cells and give the right signals for activation in a coincidental type situation.
If I were going to pick a reason it would be dysregulation of the immune system due to T cell depletion --> autoimmunity rather than the mutation hypothesis because it seems more likely.  But the mutation reason seems more of a 'VCE' type response.

[psyxwar]

Yeah that's a fair point (about it not being an autoimmune disease anymore). Thanks for the info

I find a lot of the (non-VCAA of course) model answers to be pretty bad. Like, if a question asks for how a vaccine results in life long immunity, is it not sufficient to talk about how it induces a primary immune response and thus causes the formation of memory cells (due to the B-cell specific to that antigen binding to one and proliferating)?

One of the marks in the answer is awarded for "B-cells are stimulated by Helper T cells to clone into plasma cells which then produce the antibody specifically against the injected antigen". I mean, that's very nice and all, but how is it even relevant?

tl;dr: is going on tangents the secrets to bio success? :O

[Russ]

Well the question asked for "how" the vaccine produced immunity and discussing the mechanics of that process seems important?

[simpak]

That is how the primary immune response is stimulated prior to formation of memory - the B cell won't form memory unless it gets help from the Helper T cell so I guess to get lifelong immunity in terms of antibodies it is relevant to say that T cell help is involved.  The problem is that I think there is a lot of diversity in what is taught - some will be told what you just said about general proliferation and some get more technical detail which is that if the B cell binds without T cell help it will just die instead of proliferating because it will never get a special survival signal which is provided by T cells through one of the markers they express on their surface.

You should think of it in terms of like a 1, 2, 3, 4 step by step process - what needs to happen to lead up to the point of the memory forming?  Like Russ said, you need to kind of discuss what is meant by 'primary response' - primary response is like a blanket term for a lot of individual events.

[psyxwar]

Well the question asked for "how" the vaccine produced immunity and discussing the mechanics of that process seems important?

well, yes. I meant more so talking about the production of plasma cells to produce antibodies against the antigen doesn't contribute to lifelong immunity.

[Snorlax]

So going through past VCAA exams, I came upon a question asking
Why is mDNA useful in tracking human evolutionary history, and one of the possible, suggested answers was "mDNA is inherited from the mother".
How would you get away with that? It doesn't even answer the question...

EDIT:
Or do they assume that we should elaborate on it?
I'm really confused on how the assessors want questions answered.

[vox nihili]

So going through past VCAA exams, I came upon a question asking
Why is mDNA useful in tracking human evolutionary history, and one of the possible, suggested answers was "mDNA is inherited from the mother".
How would you get away with that? It doesn't even answer the question...

EDIT:
Or do they assume that we should elaborate on it?
I'm really confused on how the assessors want questions answered.

That's a point to make, but it sounds like something is missing. Though it's handy because it allows you to track one line, without fear of crossing over etc. It's also not particularly mutable, so that's also very handy.

[Yacoubb]

So going through past VCAA exams, I came upon a question asking
Why is mDNA useful in tracking human evolutionary history, and one of the possible, suggested answers was "mDNA is inherited from the mother".
How would you get away with that? It doesn't even answer the question...

EDIT:
Or do they assume that we should elaborate on it?
I'm really confused on how the assessors want questions answered.

It would be useful because if it is only inherited maternally, then it can be tracked via the maternal line whilst mtDNA not being recombined like nuclear DNA is. But my answer to that would be the D-loop in the hypervariable region having a high mutation rate.

[vox nihili]

It would be useful because if it is only inherited maternally, then it can be tracked via the maternal line whilst mtDNA not being recombined like nuclear DNA is. But my answer to that would be the D-loop in the hypervariable region having a high mutation rate.

mtDNA is useful because of its low mutation rate. I'm not really au fait with all of it, but that's definitely an important statement to make. mtDNA has been used to track really long lineages back to the first humans.