Biochemistry, cell biology, and genetics question thread

[Nutmeg]

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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

*********

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.

 

[gotgame83]

A- increased tidal volume- (Will occur)
B- increased respiration rate (Will occur)
C- right shift of hemoglobin dissociation curve (Will occur due to 2,3 DPG)
D- increased concentration of erythropoietin in the blood. (Not enough time to occur)

So I thought D should be the correct answer for the question....

 

[Peterock]

A- increased tidal volume- (Will occur)
B- increased respiration rate (Will occur)
C- right shift of hemoglobin dissociation curve (Will occur due to 2,3 DPG)
D- increased concentration of erythropoietin in the blood. (Not enough time to occur)

So I thought D should be the correct answer for the question....

http://www.usd.edu/biol/faculty/swanson/ecophys/readings/Oxygen.html

1. increased blood oxygen carrying capacity (increased erythropoiesis) — takes weeks for full expression
2. Change in blood oxygen affinity — immediately see slight increase in affinity due to respiratory alkalosis, followed within hours by increased DPG which gives net rise in P50.

You are right, D is correct. Since 2,3 DPG is produced by the rbc's this should also be a faster response as opposed to actual rbc production etc.

Either way this question is an odd one. BTW I don't look at the question format, I just put T or F next to each answer (that way I don't get caught up on except, "not", etc questions).

 

[gotgame83]

Hmm, yea i dont like this question. It appears that it may take 2-3 days for 2,3 DPG to kick in but it takes even longer for erythropoietin to increase. So there are two bad answers. Ehh i dont know, Im not going to let kaplan win that easy, time to google some more information lol.

 

[gotgame83]

Yay! I get one extra point lol. If anyone cares to look at this question its # 211 on kaplan FL3

 

[Peterock]

Yay! I get one extra point lol. If anyone cares to look at this question its # 211 on kaplan FL3

Yeah, I think so. Maybe we should wait for a master mod person as it is now I get stuck on 13's for my practice bio so I am not infallible like some of the sdn characters.

I still think that a chemical like 2,3 DPG that is produced directly by circulating RBC's is going to be a more immediate response than the the production of extra blood cells by having the kidney release erythropoieten and then signaling the marrow etc

Simple chemical production should usually be quicker - just seems like common sense. I was really trying to find info that would correspond to the kaplan answer.

 

[medstu2006]

For the MCAT, is it necessary to know what intermediates the carbhohydrates, fats and proteins are converted into and where they enter the Krebs cycle?

 

[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?

 

[dtreese]

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.

Some of it just takes some pondering, but I'll see what I can do. I'll assume you copy of a standard velocity vs. concentration graph and a copy of a Lineweaver-Burke plot to look at while you read this.

When you look at an enzyme reaction, you're really looking at two reactions:

E+S <--> ES --> E + P

So in those rxns, E is the enzyme, S is the substrate, and P is the product. You'll notice that substrate binding is reversible, so you could say that we're looking at three possible reactions. Call the first forward reaction R1. Call the reverse of that reaction R2. Call the release of product from the enzyme R3.

So what happens with the Michaelis constant, Km, is that you make a ratio out of the rates of those three reactions to come up with a ratio for the overall reaction. That ratio is (R2+R3)/R1. So take a look at that ratio, and think about this: R2 and R3 are the two reactions that remove the substrate from the enzyme, and R1 is the reaction that binds the substrate to the enzyme. This means that Km is a ratio of separation:binding. So Km is related to the affinity of the enzyme for the substrate.

Now look at the velocity vs. concentration curve. Km is the substrate concentration at 1/2 of Vmax. Remember that Vmax is the mechanical limit of the enzyme -- it's churning out the product as fast as it possibly can. So look at a pair of enzymes, one with a high Km, and one with a low Km. An enzyme with a low Km reaches 1/2 Vmax at very low concentrations, because the enzyme has a high affinity for the substrate. An enzyme with a high Km, though, doesn't have a strong affinity for the substrate, so it takes a lot more of the substrate to get the enzyme up to 1/2 Vmax.

Now look at the Lineweaver-Burke plot of 1/Vo vs. 1/[substrate], aka the double reciprocal plot. The important things to remember about Lineweaver-Burke plots are the x and y intercepts. The x-intercept = -1/Km, and the y-intercept = 1/Vmax. Just learn these, and I'll help you make sense of them by discussing inhibition.

InhibitionThe best way to understand these graphs is to look at what happens with different types of inhibition.

First, think about competitive inhibition. You've got another substrate competing for the same enzyme. So what changes? Well, the enzyme suddenly has something else it can bind to, so its affinity for the substrate is reduced. At the same time, if you cram in enough substrate to overwhelm the competition, you can eventually reach Vmax. So in competitive inhibition, Km increases while Vmax remains the same. Look at your V/ graph, and the curve will stretch, because it takes a lot more substrate to get that Km at 1/2 Vmax. Look at your Lineweaver-Burke plot. The y-intercept stays the same because Vmax doesn't change. But Km has gone up, which means that -1/Km has gotten closer to zero, increasing the slope of the line and rotating it on the y-axis.

Now look at noncompetitive inhibition. In noncompetitive inhibition, you have something binding to another site on the enzyme, changing the structure of the binding site, and thus affecting the amount of enzyme that is able to bind substrate. This means that Vmax is reduced. Km, the affinity of the functional enzyme, remains the same, though. Looking at the V/ curve, you simply squish the maximum down. Looking at Lineweaver-Burke, Km is the same, so your x-intercept doesn't move. Vmax is smaller, so 1/Vmax is larger. This means that your line will have a higher slope and rotate on the x axis.

There are other conditions possible, but that covers the basics. If you comprehend those, you can figure out the rest on your own. Oh, and notice I didn't actually mention the Michaelis-Menten equation or the Lineweaver-Burke equation. Questions involving those are memorization w/plug&chug calculation. Understanding what happens on the graphs is much more intuitive.

 

[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.

 

[travelbug73]

Cells of the Immune System: derived from the hematopoietic stem cell

1. Lymphoid Lineage

T lymphocytes (T cells, made in the thymus)

B lymphocytes (B cells, made directly from the bone marrow)

Natural Killer cells (NK cells)

2. Myeloid lineage

Monocytes that give rise to macrophages

Langerhans cells and Dendritic cells

Megakaryocytes that give rise to Platelets

Granulocytes (eosinophils, basophils and neutrophils)


Primary lymphoid tissues: bone marrow and thymus

Secondary lymphoid tissues: spleen, lymph nodes


Leukocyte migration: T and B cells leave the thymus and bone marrow respectively as naïve lymphocytes, migrate into the blood and then into the secondary lymphoid tissue. Antigen presenting cells (APCs), such as dendritic cells, also derived from the bone marrow, migrate into tissues, take up antigen and bring it back to the secondary lymphoid tissues to present the antigen to the T and B cells. The T and B cells are now primed or activated and they migrate to the sites of infection and inflammation to mount an attack.

Immune Response

Pathogens usually have two locations: Extracellular and Intracellular

Extracellular Pathogens are targeted by antibodies by at least one of three processes: Neutralization, Opsonization and Complement Activation

Neutralization: antibody may bind to bacterial toxin and neutralize, thereby preventing the pathogen from interacting with host cells. These antibody tagged toxins are later degraded

Opsonization: Antigens are coated with antibodies and are targeted for phagocytosis.

Complement Activation: Antibodies coat bacterial cells and these antibodies act as receptors for the first protein of the complement system, eventually forming a protein complex leading usually to phagocytosis.

Antibodies in each class have different sites of action and therefore vary in their effectiveness in neutralization, opsonization and complement activation.

Intracellular Pathogens are targeted by a T-cell mediated response. There are two intracellular locations:

Cytosol (continuous with nucleus via nuclear pore): site of all viruses and some bacteria

Vesicular System (ER, Golgi, endosomes, lysosomes etc): site of some bacteria and some parasites

There are also two T cells and the intracellular location determines the type of T cell.

Cytotoxic T cells (Tc or CTL): Express CD8 and kill pathogens in cytosol

Helper T cells (Th): Express CD4 and are again of two kinds

Inflammatory Th1 that kill vesicular pathogens

Th2 (True helper cells) are involved in antibody production by B cells against T-dependent antigens on extracellular pathogens.


Both antibody (humoral) and cell-mediated responses contribute to eliminating the pathogen.

 

[QofQuimica]

Travelbug-

Thanks for writing those great posts. 👍 If you are planning to write some more, you can post them directly into the Biochem Explanations Thread. You won't be able to edit the TOC, but I'll keep adding the new posts to the TOC as needed.

 

[QofQuimica]

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.

I like your mnemonic; you should add it to the mnemonic thread on the main MCAT forum page. 🙂

 

[stoleyerscrubz]

Are skeletal muscles only activated by acetylcholine and not norepinephrine/epinephrine?

Does the phrenic nerve use acetylcholine to mkae the diaphragm contract?

Thanks!

 

[QofQuimica]

bumping this thread

 

[travelbug73]

CELL CYCLE (Mitosis and Meiosis will follow in later posts)

There are two main phases to eukaryotic cell division: DNA doubling in S (synthetic) phase and halving of that genome in M (mitotic) phase. The S and M phase are interspersed with G1 (between M and S) and G2 (between S and M) phases. Therefore, it is G1, S, G2 and M.

So, what happens at each of these phases?

G1: growth and preparation of chromosomes for replication

S: DNA synthesis

G2: preparation for mitosis

M: Mitosis

Any stage other than mitosis is usually called the interphase.

What are some of the key players in cell cycle regulation?

Cyclins:
Cyclin D (G1 cyclin)
Cyclins E and A (S-phase cyclins)
Cyclins B and A (Mitotic cyclins)

The levels of these cyclins change depending on the stage of the cell cycle.

Cyclin-dependent kinases (Cdks)

Cdk4 is a G1 dependent Cdk
Cdk2 is an S-phase Cdk
Cdk1 is an M-phase Cdk

Cdks must bind to the appropriate cyclin to be activated. Their levels remain fairly constant throughout the cell cycle. However, the rise and fall of the cyclins determines Cdks’ activation. For example, Cdk4 is only activated when the level of G1 cyclins rises and thus prepares the cell for chromosome replication.


We all know that every cell has to encounter various check points to progress through each of these phases, so what are some examples of such check points?

DNA damage checkpoints: present at G1 (p53), S phase, G2 and at mitosis (MAD)
Spindle checkpoints (proteins such as kinesin):
arrest cells in metaphase if spindle fibers not properly attached to kinetochore
block cytokinesis by detecting improper spindle alignment
induce apoptosis if damage irreparable

What is G0?
When a cell exits the cell cycle at G1, either temporarily or permanently, it is said to be in G0. Many times cells in G0 are terminally differentiated and will not enter cell cycle, while other cells such as lymphocytes will reenter cell cycle upon stimulation (presence of antigen). During G0, genes needed for mitotic division are repressed. Most cancer cells cannot enter G0 and therefore replicate indefinitely.

 

[QofQuimica]

Thanks for writing that cell cycle post, travelbug. 👍 I am going to copy it to the permanent cell bio thread so that it doesn't get buried in here.

Edit: Ok, you got it covered. Thanks again. 🙂

 

[travelbug73]

I've posted this on the Sticky (Biochem Explanations Thread) as well. I don't mean to double post but if somebody is not aware of the sticky, I don't want them to not have access to the post.

Interphase precedes both mitosis and meiosis and is the period between cell divisions during which time the chromosomes replicate and the chromosomes are not visible (loosely packed). During interphase, two pairs of centrioles lie next to each other, just outside the nucleus.

Mitosis is a process where in, one parent cell gives rise to two identical daughter cells. Mitosis can be divided into four stages: Prophase, Metaphase, Anaphase and Telophase.

Prophase: Chromosomes (two identical copies) condense, each chromosome has two arms and each copy of chromosome is called Chromatid. Spindle fibers form at centriole and centriole begin to separate. In addition, nuclear membrane disappears.

A short period just before metaphase, called prometaphase, comprises movement of centrioles to opposite ends of the cell and attachment of spindle fibers to each of the chromatids.

Metaphase: Chromosomes line up along an imaginary line, called the metaphase plate that divides the cell into two. The spindle fibers begin to pull the chromosomes to the opposite ends of the cell.

Anaphase: Spindle fibers separate sister chromatids to opposite ends of the cell.

Telophase: Chromatids, now called chromosomes move to each pole and new nuclear membranes form.

Once mitosis is complete, the rest of the cell divides, by a process called cytokinesis (division of the cytoplasm) and cell division is complete.


Meiosis is a type of cell division that is specific to reproduction and results in 4 daughter cells that have half the number of unidentical chromosomes (genetic information is contained from both parents). Meiosis is divided into two phases: Meiosis I and Meiosis II.

Meiosis I: comprises Prophase I, Metaphase I, Anaphase I and Telophase I

Prophase I: Chromosomes attach to nuclear membrane and pair up with corresponding chromosome (to from a tetrad) from the other parent. Homologous recombination occurs between chromosome pairs and genetic material exchange takes place.

Prometaphase I: Similar to prometaphase I in mitosis except, one chromosome (instead of chromatid) from the homologous pair is attached to each centriole. Therefore, 23 chromosomes (in humans) attach to fibers from one centriole and remaining 23 attach to the fibers from the other centriole.

Metaphase I: Chromosome pairs line up along the metaphase plate on either side.

Anaphase I: Chromosome pairs separate. One half of the chromosomes goes to one pole and the other half to the other pole.

Telophase I: Chromosomes reach opposite ends of the cell and a nuclear membrane forms marking the end of Meiosis I.

There is a major distinction between sperm and egg cells at this stage. While in sperm cells the cytoplasm is equally divided between the two emerging daughter cells, in oocytes, the cytoplasm is concentrated in one of the emerging daughter cells resulting in a large and a small daughter cell called the polar body.

Telophase I is followed by cytokinesis resulting in two daughter cells in case of sperms and one large cell and one small cell (polar body) in the case of the egg (primary oocyte to be precise).


Meiosis II follows a very short Interphase II but chromosome replication does not take place unlike in Mitosis and Meiosis I.

Meiosis II can also be divided into four phases: Prophase II, Metaphase II, Anaphase II and Telophase II. Meiosis II is very similar to Mitosis

Prophase II: Chromosomes condense, spindles form centrioles begin to separate and the nuclear membrane disappears. There is no homologous recombination.

Prometaphase II: Spindle fibers attach to chromatids and centrioles move to opposite ends of cell.

Metaphase II: Chromosomes align along the metaphase plate and fibers begin to pull at the chromosomes.

Anaphase II: Sister chromatids are pulled apart toward opposite ends of the cells.

Telophase II: Chromatids arrive at opposite poles, nuclear membranes form. Again, as in Telophase I, in the female cell, the emerging daughter cells will have unequal distribution of the cytoplasm resulting in one large and another small cell. The resulting large cell becomes the egg or ovum and the smaller cell is called the polar body. The first polar body formed at the end of Meiosis I also divides to form two polar bodies. Therefore, in females, at the end of Meiosis, there is one egg cell and three polar bodies.

Cytokinesis follows Telophase II to mark the completion of cell division.

Main differences between Mitosis and Meiosis I:

Prophase

Mitosis: Chromatids of chromosome begin to separate. There is no exchange of any genetic material
Meiosis I: Pairing of homologous chromosomes, tetrad formation and homologous recombination (exchange of genetic material) take place

Metaphase

Mitosis: Chromosomes line up along metaphase plate
Meiosis I: Chromosome pairs line up along metaphase plate

Anaphase

Mitosis: Sister chromatids pulled to opposite ends of cell
Meiosis I: Separation of chromosome pairs to opposite ends of cell

Telophase and Cytokinesis

Mitosis: Two daughter cells with identical chromosomes and exact number of chromosomes as parent cells
Meiosis I: Two daughter cells with chromosomes from both parents and half the number as parent cells and this is followed by Meiosis II

PS: Opposite ends of cell and opposite poles have been used interchangeably

 

[cosmicstarr]

In the PR sample Bio passages, there is a passage that deals with enzyme substrate interaction. Experiment 1 has no inhibitor and Experiement 2 has a competitive inhibitor. A graph shows reaction velocity vs. substrate concentration for Experiments 1 and 2.

Question: What would happen if the enzyme concentration were NOT kept constant during measurement of reaction velociy as a function of substrate concentration?

A. Vmax would remain constant, but V would change.
B. Vmax would remain constant, but Km would change.
C. Vmax would change, but Km would remain constant.
D. It is not possible to predict what would happen.


The answer is C., but I don't understand how Km remains constant when Vmax changes...

 

[QofQuimica]

In the PR sample Bio passages, there is a passage that deals with enzyme substrate interaction. Experiment 1 has no inhibitor and Experiement 2 has a competitive inhibitor. A graph shows reaction velocity vs. substrate concentration for Experiments 1 and 2.

Question: What would happen if the enzyme concentration were NOT kept constant during measurement of reaction velociy as a function of substrate concentration?

A. Vmax would remain constant, but V would change.
B. Vmax would remain constant, but Km would change.
C. Vmax would change, but Km would remain constant.
D. It is not possible to predict what would happen.


The answer is C., but I don't understand how Km remains constant when Vmax changes...

Vmax is enzyme concentration-dependent, which is why it changes if you change [E]. But I think you are really asking about the other part, which is why Km remains constant. This happens because Km is equal to the *ratio* of the enzyme-substrate complex's destruction/formation. So adding more enzyme will allow you to make more ES complex, but it will also allow you to destroy more of that ES complex, and the net ratio (Km) will stay the same.

Alternatively, you can consider it this way: Km can also be thought of as the concentration of substrate that results in a speed of 1/2 Vmax. But this is true only if your [E] remains constant. In this case, since you are not changing , you will not change Km, even though you are changing Vmax by changing [E].

Incidentally, unless you were given an explanation about all of this in the passage, this level of detail is way beyond what you'd be expected to know for the MCAT.

 

[cosmicstarr]

Vmax is enzyme concentration-dependent, which is why it changes if you change [E]. But I think you are really asking about the other part, which is why Km remains constant. This happens because Km is equal to the *ratio* of the enzyme-substrate complex's destruction/formation. So adding more enzyme will allow you to make more ES complex, but it will also allow you to destroy more of that ES complex, and the net ratio (Km) will stay the same.

Alternatively, you can consider it this way: Km can also be thought of as the concentration of substrate that results in a speed of 1/2 Vmax. But this is true only if your [E] remains constant. In this case, since you are not changing , you will not change Km, even though you are changing Vmax by changing [E].

Incidentally, unless you were given an explanation about all of this in the passage, this level of detail is way beyond what you'd be expected to know for the MCAT.

Thanks QofQuimica. Your *ratio* explanation helped me. I was originally thinking that a change in [E], say a reduction in [E], would have the same effect as a non-competitive inhibitor in that both instances would reduce Vmax. But now I see that in the case of the non-competitive inhibitor, the ratio is changed.

 

[QofQuimica]

bump

 

[passion2K7]

This is from cellular pathway topic...

I just wanted to know why fermentation produces less ATP's (two ATP's per glucose) compared to cellular respiration (which produces 36 total ATP's including 2 from glycolysis). Does this have to do with the fact that, in cellular respiration, electron carriers such as NADH + H & FADH2 get oxidized by the respiratory chain? Also, I don't quiet understand a statement "fermentation is an imcomplete oxidation of glucose." Can someone clarify this? Thanks!

-passion2k7

 

[QofQuimica]

I just wanted to know why fermentation produces less ATP's (two ATP's per glucose) compared to cellular respiration (which produces 36 total ATP's including 2 from glycolysis). Does this have to do with the fact that, in cellular respiration, electron carriers such as NADH + H & FADH2 get oxidized by the respiratory chain?

Yes. The NADH electrons get "wasted" in anaerobic respiration, but are used in the electron transport chain to produce ATP in aerobic respiration. Fermentation is done only to regenerate the NAD needed to continue with glycolysis. But if you look at where the majority of ATP are produced, they come from the electron transport chain. Thus, if a cell respirates anaerobically, it wastes most of the energy present in the glucose.

Also, I don't quiet understand a statement "fermentation is an imcomplete oxidation of glucose." Can someone clarify this? Thanks!

This is based on the different carbon-based products that are produced from glucose by each pathway. Anaerobic respiration oxidizes glucose up to lactic acid or ethanol. But aerobic respiration ultimately oxidizes all six carbons in the glucose as far as chemically possible, all the way up to carbon dioxide. If you look at the structures of each of these molecules, you will see that carbon dioxide is much more oxidized than either of the anaerobic compounds.

 

[QofQuimica]

bump

 

[QofQuimica]

bump

 

[QofQuimica]

bump

 

[kevin86]

1. why is dna phosphate group acidic?
Is it the the oxygens pulling all the electrons away?

2. Can someone explain to me how acidic and basic side chains of amino acids vs positive and negative charges and what kind of molecules they react with.