Leftover Biochem Posts

[Nutmeg]

All users may post questions about MCAT, DAT, OAT, or PCAT cell/molecular biology, genetics, and biochemistry here. Anatomy, physiology, development, embryology, and evolution questions should be posted in the other biology thread. We will answer the questions as soon as we reasonably can. If you would like to know what biology topics appear on the MCAT, you should check the MCAT Student Manual (http://www.aamc.org/students/mcat/s...anual/start.htm)

Acceptable topics:
-general, MCAT-level biology.
-particular MCAT-level biology problems, whether your own or from study material
-what you need to know about biology for the MCAT
-how best to approach to MCAT biology passages
-how best to study MCAT biology
-how best to tackle the MCAT biological sciences section

Unacceptable topics:
-actual MCAT questions or passages, or close paraphrasings thereof
-anything you know to be beyond the scope of the MCAT

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If you really know your cell/molecular biology, I can use your help. If you are willing to help answer questions on this thread, please let me know. Here are the current members of the Cell/Molecular Biology Team:

-Nutmeg (thread moderator): My background is in neurobiology. Please note that I am nocturnal, and generally only post between the hours of 10pm and 8am PST.

I'm going to make this thread a bit different than the others, because the material covered in the BS section is a bit different. With o-chem, gen-chem, and physics, there are a number of core concepts to understand. While there is also a lot of that in the BS, there is also a great deal of specific knowledge involved in this section (relative to the others). Test questions often introduce an experimental set-up, asking for either expected results or the interpretation of results. As such, passages might relate to advanced concepts that you are not expected to know coming into the test, and that they will explain in the passages. Any familiarity that you have with these concepts will make the test easier.

While in general this forum is designed for people studying for the MCAT, I welcome any questions relating to molecular biology, even though they might be beyond the scope of the MCAT. I know some people also like to use these threads to get help on homework questions, and I welcome that, too.

-LT2: LT2 is finishing her MS in microbiology.

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[soo21085]

I am quite new to this and still have not figured out how to post a topic under this thread. I know we have to know transcription and translation for eukaryotic organisms, but do we need to know them for prokaryotic organisms in depth? And are the eukaryotic gene expression regulations such as the TATA box important, and if not, what are some that we should definitely know?

Is cell mediated immunity specific in its action? I know that humoral immunity is highly specific due to antibodies but it's confusing me if this level of specificity is involved with T cells.

 

[Nooro]

If a postmenopausal woman is given progesterone and estrogen supplaments, what side effect will they see?

the answer was periodic menstration

I thought that when woman were impregnanted the corpus luteum produced progesterone and estrogen to maintain the endomentrium to not allow menstration. In turn inhibiting GnRH which inhibits LH and FSH? any thoughts?

 

[faluri]

Could someone please explain the Michaelis M constant and enzyme enhibition related to Km, Vmax, etc. I can't seem to find any text that explains it well.

 

[Mister Pie]

Exactly how much genetics are we supposed to know? Over on the MCAT disucssion board, people are saying that in recent years, the MCAT has focused more on genetics. The only genetics I've really covered is dominance, linked genes, punnet squares. What else is there? Hardy-Weinberg?

 

[medworm]

Well, that's what they look like to me at least...

What I'm referring to are the parallel chromosomes
with lettered genes that appear in genetics passage.

My bio classes didn't cover any MCB or genetics --
so I haven't a clue what the diagram conveys or
or how to work through the passages.

Any input is appreciated. Thanks!

 

[medworm]

Hi again, I went through the list of MCAT topics and found skimpy information in my review books or old textbooks for these. If someone could write up a quick summary on each of these topics, that'll be extremely helpful. Thanks!

Specifc coupling of free nucleic acids
Cancer as a failure of normal cellular controls
Oncogenes
Post-transcriptional control (GEC)
Genes: recombination, single and double crossovers
Prokaryotic Cell: Plasmids and extragenomic DNA
Hardy Weinberg Principle

 

[LT2]

Hi-

i don't know if you have any particular questions regarding prokayrotic plasmids and extragenomic DNA, i'd be happy to answer them.

plasmids are non-essential, circular pieces of DNA found in prokaryotes. they are commonly used in biotech in order to move genes around, for cloning, and for protein expression. they are also seen in nature and sometimes carry toxins or virulence factors. i don't know if you need to know about f' plasmids or not but they are fertility plasmids that are passed via conjugation between bugs.

if you need specifics, feel free to ask...

 

[HITMAN]

Hello,
I have a couple of quick questions pertaining to biochemistry and cell bio.

1. What is the first committed/irreversible step in the glycolytic pathway?
Is it fructose-6-phosphate to fructose-1,6-bisphosphate? What is the reasoning behind the answer? Does it have anything to do with a step being strongly exothermic?

2. In what stage of interphase are centrioles replicated?
On p.54 of my Kaplan MCAT notes it says during G1, but on p. 593 of my Cell & Molec. Bio textbook (Gerald Karp) it says at the beginning of the S phase, along with chromosome replication. I have also heard that it occurs during G2, and so I am looking for clarification on this question.

Thank you, any help is greatly appreciated.

 

[travelbug73]

Hi again, I went through the list of MCAT topics and found skimpy information in my review books or old textbooks for these. If someone could write up a quick summary on each of these topics, that'll be extremely helpful. Thanks!

Specifc coupling of free nucleic acids
Cancer as a failure of normal cellular controls
Oncogenes
Post-transcriptional control (GEC)
Genes: recombination, single and double crossovers
Prokaryotic Cell: Plasmids and extragenomic DNA
Hardy Weinberg Principle

If these questions are not answered before the end of next week (my summer II finals are next week), I can try answering some.

I do not follow what you mean by specific coupling of free nucleic acids, also can you please expand GEC?

Thank you

 

[nnguyen72]

I had trouble figuring this question out. It was found in the AAMC 7R Q. 166, part of the independent section (non-passage based)
It reads:

Embryonic mouse cells divide every 10 hours at 37 C. How many cells would be produced from an egg after three days?

A) Fewer than 50
B) Between 50 and 500
C) Between 500 and 5000
D) More than 5000

To solve this problem I first determined the numbers of hours in 3 days. So, 3 x 24 hours = 72 hours. Since the mouse cells divided every 10 hours, this meant the 72 / 10 = 7 complete cell divisions occured. I then calculated that 2 ^7 = 128 and circled answer choice (B). To my surprise, the correct answer is (D), not (B). How is this possible?

 

[nnguyen72]

Hello,
I have a couple of quick questions pertaining to biochemistry and cell bio.

1. What is the first committed/irreversible step in the glyoclytic pathway?
Is it fructose-6-phosphate to fructose-1,6-bisphosphate? What is the reasoning behind the answer? Does it have anything to do with a step being strongly exothermic?

Hitman, the production of F 1,6, Bisphosphate from F-6-P is the first irreversible step in glycolysis, according to my BioChem textbook. It has the do with the fact that the reaction happens spontaneously due the large negative delta G (free energy) ...-14.2 kJ/mol to be exact. For clarification, this reaction is spontaneous, which may or may not be "exothermic", depending on reaction conditions. Remember that G = H - TS. "H" represents the exothemic part. It quite possible to have an endothermic reaction (positive H) and still be spontaneous (negative G). Hope this helps.

 

[HITMAN]

Hitman, the production of F 1,6, Bisphosphate from F-6-P is the first irreversible step in glycolysis, according to my BioChem textbook. It has the do with the fact that the reaction happens spontaneously due the large negative delta G (free energy) ...-14.2 kJ/mol to be exact. For clarification, this reaction is spontaneous, which may or may not be "exothermic", depending on reaction conditions. Remember that G = H - TS. "H" represents the exothemic part. It quite possible to have an endothermic reaction (positive H) and still be spontaneous (negative G). Hope this helps.

Nnguyen72, thank you for your help. I also tried to answer your question, and got the exact same answer by the same reasoning. Pehaps there is an error in the answer key?

 

[gotgame83]

I had trouble figuring this question out. It was found in the AAMC 7R Q. 166, part of the independent section (non-passage based)
It reads:

Embryonic mouse cells divide every 10 hours at 37 C. How many cells would be produced from an egg after three days?

A) Fewer than 50
B) Between 50 and 500
C) Between 500 and 5000
D) More than 5000

To solve this problem I first determined the numbers of hours in 3 days. So, 3 x 24 hours = 72 hours. Since the mouse cells divided every 10 hours, this meant the 72 / 10 = 7 complete cell divisions occured. I then calculated that 2 ^7 = 128 and circled answer choice (B). To my surprise, the correct answer is (D), not (B). How is this possible?

the answer key and explanation I have say the correct answer is B

 

[faluri]

Hey dtreese.

Thanks for such a thorough answer!

 

[Mikhail]

Hello,

I have a few questions on the polypeptide structure.
The translation of polypeptide takes place on a ribosome (or polysomes) that is attached to a rough endoplasmic reticulum. When polypeptide enters the cisternae, what structure does it have? It’s definitely primary. Where does it have modifications that result in the secondary, tertiary structures? Where do 2 or more polypeptides combine to become a protein?

Thank you

 

[medworm]

specific coupling of free nucleic acids, also can you please expand GEC?

Thank you

It's in the AAMC list. I'm wondering the same too -- but at this point, I'll just ignore that.

 

[medworm]

I got stumped in one of those pedigree-type Qs where the answer was male X-link. However, not all the men were affected, so I thought it was autosomal. What am I missing?

 

[medworm]

How are cancer/oncogenes structurally different than normal genes? How is DNA replication activated? By steroids or peptides or just pure mutation? I recall reading that they have extra-long telomeres, which enable repeated replication. So they spend more time in the S phase? I really don't know anything in this area -- not sure what I need to know.

What is a double crossover? What triggers it and what are its effects? I'm assuming genetic variability.

 

[speranza]

I got stumped in one of those pedigree-type Qs where the answer was male X-link. However, not all the men were affected, so I thought it was autosomal. What am I missing?

All males do not have to be affected for a disorder to be X-linked recessive. But of the affected persons, the vast majority have to be male because they can not have a corresponding dominant gene on the X chromosome (as females do). Keep in mind that the presence of one or two affected females (who are homozygous recessive on their X chromosomes) does NOT mean that the disease does not follow X-linked recessive inheritance patterns. As long as the large majority of affected individuals are male, it is a very good indication X-linked recessiveness is the answer, but again, ALL of the males do not have to be affected (they may simply receive X chromosome from their mother that has the dominant allele). Hope this clarifies a bit.

 

[LT2]

How are cancer/oncogenes structurally different than normal genes? How is DNA replication activated? By steroids or peptides or just pure mutation? I recall reading that they have extra-long telomeres, which enable repeated replication. So they spend more time in the S phase? I really don't know anything in this area -- not sure what I need to know.QUOTE]

I don't know if this is what you're looking for, or how much this will help, and i'm a bit rusty, but i'll give it a try. there are genes called oncogenes (or c-onc for cellular oncogenes) that are players in regulating the cell cycle. certain viruses (ie retroviruses like the rous sarcoma virus) can modify these genes to create v-onc genes (viral oncogenes) that throw the cell cycle off. in v-onc genes, many times only a portion of the cellular oncogene is present. in v-onc there can be a loss of cellular control elements like promoters or repressors. also, deletions or rearrangements can be present that may affect the structure of the protein itself.

hope that made a bit of sense...

 

[totalcommand]

How are cancer/oncogenes structurally different than normal genes? How is DNA replication activated? By steroids or peptides or just pure mutation? I recall reading that they have extra-long telomeres, which enable repeated replication. So they spend more time in the S phase? I really don't know anything in this area -- not sure what I need to know.

What is a double crossover? What triggers it and what are its effects? I'm assuming genetic variability.

I don't think we really need to know much about this for the MCAT...maybe just know that the cell cycle is controlled by proteins called cyclin dependent kinases (CDKs))...and that they will spend much more time in S phase relative to the other normal stages - G1, G2, and mitosis.

...but if you're interested in more than the MCAT...(if you're not, don't read ahead! no need to waste precious brain cells remembering this stuff)

Oncogenes are simply modified "normal" genes (called proto-oncogenes). They could result from a base pair substitution, a deletion, or an insertion. Usually the product of an oncogene will create a hyper-functional protein - a protein that cannot be inactivated by the normal process. (the RAS protein is an example of this. when bound to GTP, it is in the "on" position and heavily promotes cell growth. when the proto-oncogene ras becomes an oncogene ras, oftentimes the modification results in a protein which cannot have the GTP removed. the RAS is stuck in the "on" position".)

Proto-oncogenes are akin to a the gas pedal on a car. Cancer keeps the pedal to the metal and doesn't let the gas pedal up.

DNA replication is activated by a complex pathway, but the main protein involved is the RB protein, which acts as a checkpoint before entry to S phase. Normally, RB is not phosphorylated and is bound to and inhibits a protein called E2F, which is a transcription factor for many S phase specific genes. CDKs (4 and 6) phosphorylate RB, releasing its inhibition of E2F, and thereby allow entry into S and DNA replication to occur. Many if not most cancers have some aberration in this RB pathway.

RB is called a "tumor suppressor", because it delays cell growth & replication normally. It's like the brake pedal on a car. Cancers cut the wire to the brake pedal, making it useless.

 

[jon0013]

Cell Immunity

can someone explain when the body does Humoral Mediated Immunity and when it does Cell Mediated Immunity? never really understood the difference even though i know how each one works....thanks

 

[medworm]

Thank you! That was a nice summary.

 

[medworm]

Cell Immunity
can someone explain when the body does Humoral Mediated Immunity and when it does Cell Mediated Immunity? never really understood the difference even though i know how each one works....thanks

I'll let someone else do the detailed explaining, 'cuz frankly not my forte. But if you get confused as to which one matches up with T-cells and which is for B-cells, I have a mnemonic:

T-Cell as in T-Mobile is cellular.
B-Humor as in B-rated Comedy.

Your body activates both types, often at the same time, and their actions are coordinated. For example, T-helpers solicit B-cells to bind to antigens when foreign bodies (namely viruses) are present.

I hope it's safe to say that for the MCAT, CELLULAR responds to antigenic viruses that have taken up residence in a host cell and HUMORAL responds to pathogens in the blood, lymph and tissue fluids.

And lastly, nonspecific includes complement system, interferons, natural killer cells and histamines/inflammation.

 

[totalcommand]

I'll let someone else do the detailed explaining, 'cuz frankly not my forte. But if you get confused as to which one matches up with T-cells and which is for B-cells, I have a mnemonic:

T-Cell as in T-Mobile is cellular.
B-Humor as in B-rated Comedy.

Your body activates both types, often at the same time, and their actions are coordinated. For example, T-helpers solicit B-cells to bind to antigens when foreign bodies (namely viruses) are present.

I hope it's safe to say that for the MCAT, CELLULAR responds to antigenic viruses that have taken up residence in a host cell and HUMORAL responds to pathogens in the blood, lymph and tissue fluids.

And lastly, nonspecific includes complement system, interferons, natural killer cells and histamines/inflammation.

Hey, so Cellular responds to infected human cells (virus/bacteria inside the human cell), and humoral responds to extracellular pathogens like plain bacteria?

Also, I just wanted to make clear that in this sentence...

I don't think we really need to know much about this for the MCAT...maybe just know that the cell cycle is controlled by proteins called cyclin dependent kinases (CDKs))...and that they will spend much more time in S phase relative to the other normal stages - G1, G2, and mitosis.

...Cancer cells spend more time in S relative to other cell cycle stages, but most normal cells will spend more time in G1 (or really G0) than other cell cycle stages.