Leftover Biochem Posts

[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

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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.

 

[Shrike]

What do our taste receptors actually detect?

I mean chemically, i.e.:

sweet = OH groups?
salt = ions, but which ones?
sour = protons?
bitter = ?
umami (meatiness; whatever MSG adds) (assuming this "taste" exists) = ?

 

[Shrike]

How much do I really need to know about the cellular-level energy cycles?

 

[Shrike]

What do I really need to know about organelles? Which organelles?

 

[Lindyhopper]

QofQ Thank you for your clear, well organized answer. I was wondering about your thoughts on texts, including TPR materials, that assume: that each NADH yields only 2.5 ATP and FADH2 yields only 1.5 ATP. The total would therefore, yield 30 ATP in euk. & 32 in prok. . Is this a significant discrepancy?
Also how significant is prok. anaoerbic respiration (as opposed to fermentation). My understanding is that in anaoerbic respiration, there is e- transport leading to the phosphorylation of ADP, but that some chemical other than O (often S) is the final electron acceptor.
Thanks

 

[Nutmeg]

What do our taste receptors actually detect?

I mean chemically, i.e.:

sweet = OH groups?
salt = ions, but which ones?
sour = protons?
bitter = ?
umami (meatiness; whatever MSG adds) (assuming this "taste" exists) = ?

(This is mostly pretty recent, and there are a few details that remain to be hammered out, and some of this may not be correct, but here's what I learned last year).

Sweet reception is more than just a detection of -OH groups. THere is a family of transmembrane g-protein coupled receptors called the T1Rs. The various tastes are sensed by various cells, differentiated by the type of receptors expressed in the cell.

The sense of sweetness is detected by cells that express a combination of the T1R2 and T1R3 receptors. There is a quality about the sugars that trigger the perception of sweetness such that they bind to one of each of these receptors, creating a heterodimer and trigger the cascade that makes the cell fire. The umami sense is triggered likewise by a coupling of the T1R1 and T1R3 receptors. Some cells are known to express either only T1R2 or only T1R3, and these have a low affinity detection of sugars (or perhaps there is a yet unrecognized ligand for these cells).

Sour is detected in sour-sensing cells by H+ ion blocking of the K+ channels, slowing K+ efflux and ultimately depolarizing the cell. Saltiness is detected by Na+ entering the Na+ channels and depolarize the cell.

Bitterness is mediated by several distinct receptors that bind to various types of alkaline (often amine) molecules, in the T2R family. Bitterness is usually associated with potential toxins, so many receptors detect many things.

 

[QofQuimica]

QofQ Thank you for your clear, well organized answer. I was wondering about your thoughts on texts, including TPR materials, that assume: that each NADH yields only 2.5 ATP and FADH2 yields only 1.5 ATP. The total would therefore, yield 30 ATP in euk. & 32 in prok. . Is this a significant discrepancy?
Also how significant is prok. anaoerbic respiration (as opposed to fermentation). My understanding is that in anaoerbic respiration, there is e- transport leading to the phosphorylation of ADP, but that some chemical other than O (often S) is the final electron acceptor.
Thanks

I am not familiar with the TPR materials, so I am not sure how they came up with those numbers that each NADH yields 2.5 ATP instead of 3. Maybe Shrike or another TPR instructor can chime in on this one? But in the whole scheme of things, I would say it is less important to know how many ATP each NADH yields than it is to know how many NADH are formed at each stage. It is entirely plausible that both numbers are not perfectly accurate, because there are probably other factors that affect the efficiency of the entire respiration process. (Biological processes are always more complex than an introductory level textbook makes them out to be. 😛 ) But of course we are way over the level of knowledge you are expected to have for the MCAT here.

For your second question, I think you are asking about sulfur-reducing bacteria? (They make H2S rather than H2O.) If so, you do not need to know about this at all for the MCAT; if they asked you any questions about it, it would be explained to you in a passage.

 

[gotgame83]

There has been recent debate as to whether or not NADH produces 3ATP and FADH2 yields 2 ATP. The recent texts seems to say that the actual ATP produced is slightly less then the previously accepted values. However, I was told that for the MCAT we should use the old numbers of 3 and 2.

 

[psiyung]

QofQ Thank you for your clear, well organized answer. I was wondering about your thoughts on texts, including TPR materials, that assume: that each NADH yields only 2.5 ATP and FADH2 yields only 1.5 ATP. The total would therefore, yield 30 ATP in euk. & 32 in prok. . Is this a significant discrepancy?
Also how significant is prok. anaoerbic respiration (as opposed to fermentation). My understanding is that in anaoerbic respiration, there is e- transport leading to the phosphorylation of ADP, but that some chemical other than O (often S) is the final electron acceptor.
Thanks

This really is not required for the MCAT, but if you are interested in knowing, the debate is still going on.

It all boils down to the P/O ratio. The P/O ratio refers to the number of molecules of ATP formed in oxidative phosphorylation for every two electrons flowing through a defined segment of the electron transport chain. There is still some debate regarding this value.

10H+ are transported out of the matrix for every two electrons that pass from NADH to O2

4 H+ are transported into the matrix for every ATP synthesized
P/O = (1 ATP/4H+)*(10H+/NADH)*(1 NADH/2e') = 2.5 ATP/2e'

This is more or less close to the 3 ATP's for each NADH that enters oxidative phosphorylation quoted previously

 

[blankguy]

For all of the pre-health tests (MCAT, PCAT, DAT, and OAT), you should be able to follow the generation of ATP in each step, and also the energy carrier reduction (NAD and FAD) in each stage. You do NOT need to memorize any enzymes or pathway intermediates; they will make you do that in your professional school biochem class. You should also know that oxygen is the final electron acceptor of the electron transport chain, and that anaerobic respiration is insufficient to sustain human life. In addition, fermentation produces lactic acid as a byproduct in humans, and ethanol in yeast. Finally, you should know where in the cell each stage of respiration occurs. Here is a list of the energy conversions for each stage and where in the cell they take place:

Glycolysis: (anaerobic, occurs in the cytoplasm)

• 2 net ATP (4 total made, but 2 needed to complete this stage)

• 2 NADH produced (making 4 ATP in ETC for eukaryotes and 6 ATP for prokaryotes)

Fermentation: (anaerobic, occurs in the cytoplasm)

• 0 ATP; its main purpose is to reoxidize the NADH produced in glycolysis

Pyruvate Decarboxylation: (aerobic, occurs in the cytoplasm for prokaryotes, mitochondrial matrix for eukaryotes)

• 0 ATP produced

• 2 NADH produced (making 6 ATP in ETC)

TCA Cycle: (aerobic, occurs in the cytoplasm for prokaryotes, mitochondrial matrix for eukaryotes)

• 2 ATP produced

• 6 NADH produced (making 18 ATP in ETC)

• 2 FADH2 produced (making 4 ATP in ETC)

Electron Transport Chain (ETC): aerobic, occurs across the inner cell membrane for prokaryotes, inner mitochondrial membrane for eukaryotes

• NADH oxidation back to NAD and FADH2 oxidation back to FAD occur along with ATP production, allowing the earlier stages to continue

Summary: 36 net ATP produced in eukaryotes, 38 net ATP produced in prokaryotes (because the electrons from the NADH produced from pyruvate decarboxylation do not have to be transported across the mitochondrial membrane in prokaryotes; doing this causes a net loss of two ATP in eukaryotes)

I was thinking about making index cards to memorize. Should I just study as to what goes in and what it ends up making. Ex: Krebs starts with Pyruvate---> ATP, etc... or should I put more detail. I'm still struggling as to how to best tackle memorize these.

 

[Lindyhopper]

I often see stated as a fact that triaclglycerol is the body energy storage and that it supplies the most ATP per carbon. TPR has a straight forward question reinforcing this "fact". When I do the math, I can't make it add up.

Using the simple conversion of 3 ATP per mitoch. NADH & 2 ATP per FADH2. Each glucose molecule yields 36 ATP or 6 ATP per C.
For every 2 Cs in the fatty acid chain we get 1 turn of the Krebs cycle. Each turn of the Krebs cycle yield 3 NADH, 1 GTP, 1 FADH2 for a total of 12 ATP. Or 6 ATP per C. The glycerol will also be converted to PGAL and enter pathway at a point that seems to also generate 6 ATP.

I can see that the C of triaclglycerol with many bonds to H and few to O is more reduced than the C of glucose, But why doesn't my math confirm this by yielding more ATP per C? Can ATP possibly be generated by the beta- oxidation of fatty acids to acetyl-CoA?

 

[Nutmeg]

I often see stated as a fact that triaclglycerol is the body energy storage and that it supplies the most ATP per carbon. TPR has a straight forward question reinforcing this "fact". When I do the math, I can't make it add up.

Using the simple conversion of 3 ATP per mitoch. NADH & 2 ATP per FADH2. Each glucose molecule yields 36 ATP or 6 ATP per C.
For every 2 Cs in the fatty acid chain we get 1 turn of the Krebs cycle. Each turn of the Krebs cycle yield 3 NADH, 1 GTP, 1 FADH2 for a total of 12 ATP. Or 6 ATP per C. The glycerol will also be converted to PGAL and enter pathway at a point that seems to also generate 6 ATP.

I can see that the C of triaclglycerol with many bonds to H and few to O is more reduced than the C of glucose, But why doesn't my math confirm this by yielding more ATP per C? Can ATP possibly be generated by the beta- oxidation of fatty acids to acetyl-CoA?

Yes, it can and is, and for exactly the reason you state. Before the fat is metabolized in the Citric Acid Cycle, it must be converted to Acetyl CoA. This is done by beta oxidation, which produces FADH2 and NADH while consuming one ATP per pair, which gives another 4 ATP per pair of carbon molecules. The total then is 4 from beta oxidation plus 12 from Krebs cycle for a net of 16 ATP per two carbons, or about 8 ATP per carbon.

 

[LT2]

in response to lindyhoppers question regarding anaerobic respiration in prokaryotes, many bacteria create energy which works somewhat similarily to aerobic respiration. you seem to have the correct idea. in aerobic respiration, bacteria utilize oxygen as a terminal electron acceptor. in anerobic respiration, they use things like nitrate, sulfate, etc. it is not as efficient as aerobic respiration, however it is far more energy efficient than fermentation. just know that aerobic respiration, anaerobic respiration and fermentation are all separate things (and very basically, why). hope this helps a bit.

 

[mostwanted]

Hi Q of Q, can you please go over the repressible and inducible operons and can you also please go over the fungi stuff we need to know? Thank you

 

[blankguy]

Could somebody clarify what the P, A, E sites are in the translation.
I got the P site is when the methione codon(initialtion codon) hooks up with the ribosome(rRNA and proteins) in the mRNA. A site is the same for the tRNA(anticodon) which pairs with the mRNA and the E site is the next codon after the start codon, when the actual elongation starts and the actual sequence begins. 😕

 

[mustangsally65]

I PMed one of the thread moderators of this sub-forum, and when this mod didn't know the answer I was told to post this in the biochem thread. I saw the disclaimer at the top saying not to post embryology questions here, so I hope this isn't in the wrong place.

When a zygote divides in the early stages to produce identical twins, is it possible for the split to be uneven? Also, I've read that often the splitting is caused by problems with the genes, and the zygote is trying to dispense of the bad genes to produce a more viable embryo. If one twin dies in-utero, and then has a lot of health problems later in life, could this be because of the split of the zygote? Because there were problems with the embryo to begin with, and nature tried to remedy that, but it didn't work out all the way and the embryo actually survived and was born?

I realize this isn't really MCAT related, and it's impossible to identify the cause of different health problems. I know someone who has been told he has bad genes by his doctor, while his siblings have no health problems at all. I was just curious if someone could point me towards some research in this area, or answer my question.

Thanks!

 

[LT2]

The ribosome sites are as follows:

A site is the "acceptance" site where incoming tRNA's go before their amino acid gets tacked onto the growing chain (it's like the on deck circle at a baseball game)

the P site is the "peptide" site where the amino acid gets tacked onto the chain. the growing amino acid chain elongates and stays here.

the E site is the last site, the "empty" site where the empty tRNA's are released from the ribosome.

make sense??

 

[blankguy]

The ribosome sites are as follows:

A site is the "acceptance" site where incoming tRNA's go before their amino acid gets tacked onto the growing chain (it's like the on deck circle at a baseball game)

the P site is the "peptide" site where the amino acid gets tacked onto the chain. the growing amino acid chain elongates and stays here.

the E site is the last site, the "empty" site where the empty tRNA's are released from the ribosome.

make sense??

Thanks a lot 👍
I didn't find the EK to be very clear on this.
empty tRNA's are the portion of the tRNA that is done or "use up" right? after that portion is translated.

 

[LT2]

yes, "empty" tRNA's are tRNA's that have no amino acids attached to them, so i suppose they could be considered "used up".

i'll try to do a blurb on transcription and translation sometime soon...

 

[blankguy]

yes, "empty" tRNA's are tRNA's that have no amino acids attached to them, so i suppose they could be considered "used up".

i'll try to do a blurb on transcription and translation sometime soon...

Thanks.
If somebody could do the same for the cellular respiration, because it doesn't seem like we have to know that much about the krebs cycle with the exception of Acetyl CoA, pyruvate, and NADH. Also the electron transport chain with the ATP synthase with the proton motive force.

 

[Lindyhopper]

LT2, thanks for that nice summary on "operators" control of the operon. I know it is hard to say ALWAYS in biology (Just too much damn diversity) but is it generally true that:
Activation of an inducible operon, like the lac operon, is induced by the release of the repressor from its OPERATOR, while activation of a repressible operon, like trp, is repressed by the binding of a repressor to its operator.

RE the lac operon, I would like to point out, that there is also an activator that binds, not at the operator site, but just upstream of the promoter at the CAP binding site. CAP the "catabolite activator protein" is activated by cAMP.
low glucose levels leading to high cAMP levels, and therefore, the activation & binding of CAP.
Therefore, if glu levels are high, & lac are low, the CAP activator does not bing and the repressor stays bound to the operator resulting in no transcription.
If Glu & lactose levels are both high, the CAP activator does not bind, but the repressor is freed from the operator resulting in low levels of transcription.
If Glu level are low but Lac is high - The low Glu levels result in high levels of cAMP resulting in the activation of CAP. The lactose will induce the release of the repressor from the OPERATOR resulting in high levels of transcription.

 

[TheGuy2000]

Can I get some help with the immune system? T cell mediated vs. B-cell mediated methods of fighting off pathogens. Primary vs. secondary action, and to what extent we have to know this stuff for the MCAT. It seems that T-cell is for extracellular pathogens, while B is for intracellular, while their methods are very similar. Just need some boning up on my immunology.

 

[LT2]

B cells make antibodies, not T cells!!

For Humoral Immunity:
Antibodies (also known as Immunoglobulins) neutralize toxins, bacteria, etc (in a matter of speaking). They have two heavy chains and two light chains. within these chains are constant regions and a variable regions. the constant region defines the "type" of antibody (IgM, IgA, IgD, IgG, and IgE), and the variable region is specific for epitopes of the toxin, bacteria, etc. B cells are derived from bone marrow and they produce antibodies when they encounter an antigen. this is the primary response (and is relatively slow 7-10 days). The original proliferation of B cells in response to the antigen become memory cells. when the body encounters the antigen again, these memory cells activate and produce antibodies quickly. this is the secondary response.

Cell-mediated Immunity:
This type of immunity is regulated by T cells (which also come from bone marrow). Cell mediated immunity is typically used in response to viral infections. There are a couple of types of T cells, cytotoxic T cells, suppressor T cells and helper T cells (these help activate the B cells mentioned above). T cells secrete interferons and cytokines that help deal with infection. T cells are also responsible for inflammatory response.

Hope this helps...

 

[sweetstuff25]

B cells make antibodies, not T cells!!

For Humoral Immunity:
Antibodies (also known as Immunoglobulins) neutralize toxins, bacteria, etc (in a matter of speaking). They have two heavy chains and two light chains. within these chains are constant regions and a variable regions. the constant region defines the "type" of antibody (IgM, IgA, IgD, IgG, and IgE), and the variable region is specific for epitopes of the toxin, bacteria, etc. B cells are derived from bone marrow and they produce antibodies when they encounter an antigen. this is the primary response (and is relatively slow 7-10 days). The original proliferation of B cells in response to the antigen become memory cells. when the body encounters the antigen again, these memory cells activate and produce antibodies quickly. this is the secondary response.

Cell-mediated Immunity:
This type of immunity is regulated by T cells (which also come from bone marrow). Cell mediated immunity is typically used in response to viral infections. There are a couple of types of T cells, cytotoxic T cells, suppressor T cells and helper T cells (these help activate the B cells mentioned above). T cells secrete interferons and cytokines that help deal with infection. T cells are also responsible for inflammatory response.

Hope this helps...

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.

 

[LT2]

Cell mediated immunity is non-specific in that the products secreted (interferons, etc) will kill what ever is in the vicinity. They are also somewhat involved with humoral immunity in that they activate B cells to start making antibodies. so they are technically non-specific, but they dabble in both modes of immunity.

hope that helps...

 

[blankguy]

Cell mediated immunity is non-specific in that the products secreted (interferons, etc) will kill what ever is in the vicinity. They are also somewhat involved with humoral immunity in that they activate B cells to start making antibodies. so they are technically non-specific, but they dabble in both modes of immunity.

hope that helps...

But they have proteins on their membranes that have to match to the antigen don't they?

 

[LT2]

yes, the t cells recognize antigens (specifically) but the response (ie IFN's etc) are not specific.

 

[blankguy]

I am confused as to how I should understand the ribosomes.These are the two ways that I am thinking of them just tell me which is correct.

1. The major components(large, small subunits and the rRNA) are made in the nucleolus which get "activated" in the cytosol by the substances contained in the cytosol and do their stuff eventually "depositing" the synthesized protein into the rough ER.

2. The rRNA are made within the nucleolus and move to the cytosol which combines with the subunits and get activated in the cytosol, and do the same as above. The rRNA acts as a key "turning on" the ribosome.

Which one is the closest representation of the Ribosomes?

BTW I am beginning to understand why membranes are key in Eukaryotes aside from being the distinguishing feature from Prokaryotes. 👍

 

[bug22catch]

Just wondering if anyone had advice on who best covers molecular biology --Kaplan, TPR, EK -- because I know the MCAT is increasingly slanted that way and I didn't know if the courses had changed their material accordingly.

Thanks.

 

[myfavred]

I am confused as to how I should understand the ribosomes.These are the two ways that I am thinking of them just tell me which is correct.

1. The major components(large, small subunits and the rRNA) are made in the nucleolus which get "activated" in the cytosol by the substances contained in the cytosol and do their stuff eventually "depositing" the synthesized protein into the rough ER.

2. The rRNA are made within the nucleolus and move to the cytosol which combines with the subunits and get activated in the cytosol, and do the same as above. The rRNA acts as a key "turning on" the ribosome.

Which one is the closest representation of the Ribosomes?

BTW I am beginning to understand why membranes are key in Eukaryotes aside from being the distinguishing feature from Prokaryotes. 👍

The ribosomal subunits are synthesized in nucleolous and assembled when they attach to mRNA. They can be found both in cytosol and ER. The ribosomes in the cytosol make proteins to be used in the cell and the other to be exported. Hope that helped.

 

[QofQuimica]

Not to be a thread Nazi, but perhaps issues of blood vessels would be more appropriate for the organismal biology thread...

I agree. I'm moving those posts to the organismal bio thread: http://forums.studentdoctor.net/showthread.php?t=207484 Posters, please post about systemic level biology in that thread, and only post about cellular/molecular level biology here.

 

[Lindyhopper]

The ribosomal subunits are synthesized in nucleolous and assembled when they attach to mRNA. They can be found both in cytosol and ER. The ribosomes in the cytosol make proteins to be used in the cell and the other to be exported. . .

I wanted to elaborate on "myfavred" nice concise statement. Translation begins on a free floating ribosome in the cytosol. If the nascent polypetide expresses a hydrophobic SIGNAL SEQUENCE in the first 16-30 amino acids, a signal recognition particle (SRP) will carry the entire complex to the ER. The growing protein will either be inserted into the ER lumen or threaded through the membrane of the ER.
What peptides have the SIGNAL SEQUENCE, & thus will be translated at the ER?
Proteins destined to be secreted, or end up in the "secretory pathway" will have the SIGNAL SEQUENCE. These include polypeptides that will eventually be in the lumen, or membranes of the ER, Golgi, lysomes, plasma membrane, as well as all secreted proteins.

What polypeptides will be translated in the cytosol because they lack the hydrophobic signal sequence?
Pretty much all the rest, including, proteins that will "live" in the nucleus, cytolsol, & mitochondria.

 

[Lindyhopper]

. . . I don't think you're responsible for the intricate details regarding the signal sequence and polypeptide recognition.

I'm not sure just what level will ultimately be tested, but, this level of detail is taught by TPR & a similiar level is presented in EK's book.
I think understanding the start of the secretory pathway is a pretty fundamental step in cell bio.

 

[Lindyhopper]

. . . They can be either found free in the cytoplasm or attached to the ER which is then called the RER. . .

A good point to keep clear is that translation begins on ribosomes in the cytoplasm. It is only if the nascent polypeptide is destined to enter the secretory pathway will the ribosome/mRNA complex be taken to and become attached to the ER.
Your summary was simple & good, but at TPR (where I teach MCAT bio) we stress the above point.

 

[Lindyhopper]

Travelbug that's definately the post of the week!
I've always been a little cloudy on enhancers. I assume that enhancers are sequences of DNA. To enhance or lessen transcription, must a protein bind to the enhancer? Are these proteins called "enhancer elements"?
In the case of enhancers thousands of bp from the promoter what possible mechanism can enhance the binding of TFs? Does the chromatin bend to put the enhancer elements in physical contact with the basal TFs?
In the case of enhancers within the promoter- How are they different from sequence specific TFs?

Any guidance would be welcome.

 

[travelbug73]

Reply to Lindyhopper

I assume that enhancers are sequences of DNA. To enhance or lessen transcription, must a protein bind to the enhancer? Are these proteins called "enhancer elements"?

Yes, enhancers are sequences of DNA that enhancer binding proteins or enhancer elements bind to. In addition, it is possible (and more often the case) that these enhancer binding proteins also bind to TFs present in the promoter region, thereby creating a loop, like you said.

In the case of enhancers thousands of bp from the promoter what possible mechanism can enhance the binding of TFs? Does the chromatin bend to put the enhancer elements in physical contact with the basal TFs?

Look above

In the case of enhancers within the promoter- How are they different from sequence specific TFs?

Enhancers within or outside of promoter region are not TFs per se but require the binding of TFs. The role of enhancers is to stimulate transcription, often in differentiated cell or tissue types, thereby making it cell or tissue specific transcription.

I hope I have answered your questions, if not, please feel free to ask.

Thank you

 

[Lindyhopper]

Nondisjunction the failure of homologous chromsomes to successfully seperate results in diseases such as trisomy 21 (Down's Syndrome) & Turner Syndrome (XO).
When does this failure take place? There would seem to be two possible candidates. In Anaphase I it seems quite possible that the homologous chromosomes could get tangled, resulting in the imperfect seperation.
In Anaphase II when the sister chromatid are seperated, it seems possible that an inappropriate split at the centromere could result in both sister chromatids going to same gamete.

 

[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?

 

[travelbug73]

Nondisjunction the failure of homologous chromsomes to successfully seperate results in diseases such as trisomy 21 (Down's Syndrome) & Turner Syndrome (XO).
When does this failure take place? There would seem to be two possible candidates. In Anaphase I it seems quite possible that the homologous chromosomes could get tangled, resulting in the imperfect seperation.
In Anaphase II when the sister chromatid are seperated, it seems possible that an inappropriate split at the centromere could result in both sister chromatids going to same gamete.

Nondisjunction could occur during mitosis, meiosis I or meiosis II. However, monosomies and trisomies are more common because of nondisjunction during meiosis than mitosis and more so during meiosis I than meiosis II.

 

[Lindyhopper]

Hi,
In incomplete dominance, the dominant allele is only partially expressed. The classic example is the red rose being incompletely dominant over the white rose resulting in pink offspring.
In codominant alleles both alleles are expressed. One common example is the ABO blood types.
The other common example of codominance, fur color, is less clearly different than incomplete dominance. If one expresses both co-dominant allele for say brown & red fur the result is sort of a "blend". Does anyone know how on a physical level this "co-dominant" expression is different from the incomplete dominance seen in the "blended" pink rose. In the co-dominant fur, are alternate hairs brown & red? Or perhaps, are both pigments translated in each hair but our eyes see a blend? Or something else?

 

[Tracy47]

Hi, Could someone explain reciprocal cross? 😳 Also, explanations & tips with reading pedigrees would be really helpful! Thanks!

 

[gotgame83]

Hi, maybe someone can clarify this.
-A mountain climber living at sea level ascends to a very high altitude during the course of a day long climb. By the end of the day all of the following acclimazations will occur EXCEPT:

A- increased tidal volume
B- increased respiration rate
C- right shift of hemoglobin dissociation curve
D- increased concentration of erythropoietin in the blood.

The answer they give is C

However I picked D. At the end of the climb 2,3 DPG should be increased thus shifting the curve to the right. The purpose of 2,3 DPG is to allow for a better deliver of oxygen to the muscles until erythropoeitin can increase which takes a few days. It has been a while since i delt with biochem so if someone can help out this would be appreciated.

(Im hoping that Kaplan made a mistake so I get a 12 instead of an 11 haha)

 

[Peterock]

http://us.commercial.lifefitness.com/content.cfm/exerciseataltitude
"Within 24 to 48 hours after exposure to altitude, the hormone erythropoietin is secreted from the kidneys. This hormone stimulates the bones to increase red blood cell production, thereby enabling the blood to carry more oxygen. At moderate altitudes of 7,000 feet, this acclimatization may take about two weeks. For higher altitudes, acclimatization will take several weeks."

D is wrong b/c the question states a one day hike which is a 12 hour max event.

As far as C goes, if the curve is shifted towards the right, this means that there would be less hemoglobin affinity for oxygen. This would make sense b/c it means that hemoglobin would give up O2 to the tissue at a greater rate.

Hi, maybe someone can clarify this.
-A mountain climber living at sea level ascends to a very high altitude during the course of a day long climb. By the end of the day all of the following acclimazations will occur EXCEPT:

A- increased tidal volume
B- increased respiration rate
C- right shift of hemoglobin dissociation curve
D- increased concentration of erythropoietin in the blood.

The answer they give is C

However I picked D. At the end of the climb 2,3 DPG should be increased thus shifting the curve to the right. The purpose of 2,3 DPG is to allow for a better deliver of oxygen to the muscles until erythropoeitin can increase which takes a few days. It has been a while since i delt with biochem so if someone can help out this would be appreciated.

(Im hoping that Kaplan made a mistake so I get a 12 instead of an 11 haha)

 

[gotgame83]

Thank you for responding but it says EXCEPT lol. Therefore a one day climb ISNT enough time to make D true... which is my reasoning.

 

[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?