AAMC FL 2-BIO/BIOCHEM Section Questions/Doubts

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svpatel
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Joined: Wed Jan 15, 2020 8:07 pm

AAMC FL 2-BIO/BIOCHEM Section Questions/Doubts

Post by svpatel » Sat Mar 21, 2020 3:17 pm

17. Figure 1 shows that reducing agents separate subunits of Protein X. I get that! This indicates that subunits of Protein X are linked together by disulfide bonds which implicate the thiol groups of cysteine residues. Why is that? I don't understand. I know Met doesn't form disulfide bonds and so picked ans B. But rest is confusing.

21. Do I have to know GAPDH, the enzyme encoded by the tdh2 gene, is a glycolytic enzyme that catalyzes the reversible conversion of glyceraldehyde-3-phosphate to 1,3-bisphosphoglycerate? Seems too specific. Is there a better way to ans this?

24. How do I know that I is also impt in checking the ROS in yeast here. I picked RN II, but I am unsure about how I and III will be impt in anazlying the effect of ROS on yeast lifespan and how do I get this info from the passage?

30. Q said a drug for typhoid fever is not working. This is bc there would be selection for drug resistance in: ans) S.typhi bacteria that causes typhoid. My incorrect ans:) resistance for drug in WT homozygotes. Why my ans wrong? Ppl normally do get resistance to taking drugs and say that drug doesn't work on me, I have to take higher doses or diff drug. I am lost as to the bacteria bcms resistant to the drug.

33. why is the and C? The passage said that releasing factors don't stimulate LH release, but modulate sec cells to GnRH. So I picked D. But C said factor(NPY) modulate the relase of LH. This seems counterintuitive. What should I do to avoid mistakes like these bc I know at the end we are trying to measure LH.

37. Why did we divide 7/5 and not the other way around to get the ans? And after didving 7/5, I got 1.4. How does that mean the ans is 48%. I don't get how that math works out.
NS_Tutor_Mathias
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Joined: Sat Mar 30, 2019 8:39 pm

Re: AAMC FL 2-BIO/BIOCHEM Section Questions/Doubts

Post by NS_Tutor_Mathias » Sun Mar 22, 2020 9:41 pm

#17:
Oxidizing environments promote the formation of disulfide dimers (also called cystine, not to be confused with cysteine, which is the monomeric form). For reference:
https://en.wikipedia.org/wiki/Glutathione_disulfide

The link explains this property in context of a very common biological called glutathione, that makes use of cysteine's ability to act as a reducing agent (read: become oxidized) to control the chemical environment of the cell - and at the same time be regenerated easily at a later point in time. I have also attached an image of this in action.
glutathione.png
(46.26 KiB) Not downloaded yet
Also, keep in mind that a basic environment is a reducing one and an acidic environment an oxidizing one.

#21:
You are responsible for ALL substrates of glycolysis, krebs, ETC at all times, including the enzymes. You want to also know those of beta oxidation, fatty acid synthesis, glycogenolysis, gluconeogenesis fairly well.

Since the MCAT is not too heavy on pure rote, there is little point to purely memorizing the name. But since you should be familiar with chemical nomenclature, you can quickly reconstruct what the function of GAPDH is:
- Glyceraldehyde-3-phosphate is a key glycolysis substrate (one of two products of the actual glycolytic step, catalyzed by aldolase)
- A dehydrogenase necessarily oxidizes it's substrate and will almost certainly output a reduced electron carrier (provided the reaction is happening 'forward', in according with the enzyme name)
- only option B and C even mention the molecule the enzyme is named after
- Option C is half the reversible reaction that aldolase catalyzes

Biochemical pathways can be daunting to learn, but I usually recommend chunking & sub-chunking:
1. Make lists of substrates, then memorize them 3-4 at a time (and then practice just reciting them - first 3 at once, then 6, then 9, then 12 etc)
2. Now do the same for the enzymes, but insert them into your substrate list (so "Glucose -> hexokinase -> Glucose-6-phosphate") etc.
3. Now go back and draw each substrate. This takes a while, but will make all the work you did beforehand settle in
4. Now just go right ahead and draw them one more time, ideally completely from memory, and if that is still too easy, link a few pathways together.

Throughout all this, content connections should become obvious and names become significantly less daunting. It will become somewhat obvious if you think about the name 'alpha-keto-glutarate' what the underlying structure is, and what the alpha-keto-glutarate dehydrogenase complex might do (particularly if you know what succinate looks like). B&B is a little special on the MCAT in that it is taken quite seriously and features the greatest depth of content background.

#24:
Hydrogen peroxide is a ROS, as is any peroxide. This question simply requires knowing what a reactive oxygen species (ROS) is - and that antioxidant enzymes are those that catalyze the conversion of ROS to biologically inert molecules.

#30:
People don't get resistant to antibiotics, bacteria do. CFTR is a human gene. Answer choice B also does not say 'resistance' and is purposefully a meaningless answer. The MCAT generally doesn't make mistakes of this magnitude, if an answer choice is nonsensical, it is so by design.

Further, even if one were to assume it said resistance, it contains a fundamental misunderstanding of selection: Individuals cannot, do not, ever, EVER (laser-print this on the inside of your eyelids) evolve. Additionally, nor could a population of homozygotes evolve towards anything as long as they stay homozygotes (meaning in the absence of mutation and really long timelines).

Bacterial populations on the other hand mutate frequently and tend to be genetically diverse (as they have additional methods of transmitting genetic information, such as horizontal transfer). Repeated exposure to antibiotic courses can kill predominantly those bacterial populations that are vulnerable to the antibiotic, and leaving those least susceptible in place. Very often, these bacterial antibiotic resistance genes come with a high metabolic price, and in the natural environment the populations expressing these are heavily out-competed by virtually everything else. This balance tends to shift and select for (over many generations) the more antibiotic resistant populations when exposure to those antibiotics is common.

(This is also why rotations of antibiotics that target different components of prokaryotic metabolism can be effective against previously resistant populations. Say why sulfonamides or tetracyclines may be effective after penicillins failed for a particular infection)

#33:
They don't stimulate it alone. The passage states that neuromodulators enhance or inhibit the response of secretory cells to GnRH. The study was not testing whether the hypothalamus itself makes more GnRH in response to GnRH (that was neither a hypothesis, nor would this testing show that) but whether the anterior pituitary makes more LH in response to GnRH when NPY is simultaneously added. This is why they added NPY by itself (observing no difference from control) and GnRH itself (baseline GnRH response) and then both (modulated response).

1 - [(Modulated response)/(Baseline)]

A percentage increase means "new value/baseline"-1 * 100%.

If toilet paper costs 2 dollars in February and 20 dollars in March, then that is a 900% increase (20/2 -1 * 100% = 900%).

Another way to do this is to just take the change and divide that by the baseline. So in this case 18/2 * 100% = 900%.

(In the actual problem: 7 - 4.75 = 2.25
2.25/4.5 = 0.5
0.5 * 100% = 50%

Roughly a 50% increase)
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