Biochemistry, cell biology, and genetics question thread

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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
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-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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How does the neurotransmitter travel across the cleft? is it diffusion, brownian movement, or both? I'm getting conflicting results on google. Also, is there a better explanation for what brownian movement is - other than that it's the "random movement of molecules"?

thanks:)

don't get too hung up on the detail. Diffusion is passive transport down a concentration gradient (or some sort of gradient) so, assuming neurotransmitters get released from the presynaptic neuron into the synaptic cleft which has no neurotransmitters in it at the time, the neurotransmitters would move via diffusion. Now even though the particles may be moving down their concentration gradient, it is incorrect to assume that they just move from one point to another directly like cars on a street. Particles interact with everything around them and are in reality subject to many different kinds of forces and such, which is essentially brownian motion.

I think what's important about brownian motion is to understand that even though you may have a bulk flow of particles, that is when summed up your particles are moving in a specific direction, each individual particle is moving about a little more randomly than that.
 
don't get too hung up on the detail. Diffusion is passive transport down a concentration gradient (or some sort of gradient) so, assuming neurotransmitters get released from the presynaptic neuron into the synaptic cleft which has no neurotransmitters in it at the time, the neurotransmitters would move via diffusion. Now even though the particles may be moving down their concentration gradient, it is incorrect to assume that they just move from one point to another directly like cars on a street. Particles interact with everything around them and are in reality subject to many different kinds of forces and such, which is essentially brownian motion.

I think what's important about brownian motion is to understand that even though you may have a bulk flow of particles, that is when summed up your particles are moving in a specific direction, each individual particle is moving about a little more randomly than that.


sounds good and makes perfect sense, thank you very much:):luck:
 
I know this was covered before somewhere around here. Wiki says:

"Most bacteria have a single circular chromosome"

I was under the impression that bacteria had circular double stranded DNA - or is that what wiki is implying?

thanks :)
 
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I know this was covered before somewhere around here. Wiki says:

"Most bacteria have a single circular chromosome"

I was under the impression that bacteria had circular double stranded DNA - or is that what wiki is implying?

thanks :)
Yeah. And just a heads up, although you probably know this, I wouldn't use Wiki as answers to questions like these. Wiki has competencies in areas, but I wouldn't trip myself up over dilemmas between what you know and wiki. Wiki is written by us, and so it has the potential of not being particularly clear in certain areas because of that.

So, it is circular, ds. :thumbup:
 
Yeah. And just a heads up, although you probably know this, I wouldn't use Wiki as answers to questions like these. Wiki has competencies in areas, but I wouldn't trip myself up over dilemmas between what you know and wiki. Wiki is written by us, and so it has the potential of not being particularly clear in certain areas because of that.

So, it is circular, ds. :thumbup:

thank you very much, and thanks for the heads up on wiki. I know what you mean - I've found too many errors in the past. However, I always find myself coming back to it for some reason:oops:

:luck:
 
Hello, I am looking for someone who is a doctor, or someone who knows anything about cloning. I am young reporter looking to write a full article on human cloning. I would like to know everything a doctor, or anyone here knows on the subject. I would like to know:

1) How does this technology work?
2) What are some benefits for patient care?
3) What are some ethical dilemmas this may pose
4) What are possible uses for this technology?

Anything anyone can tell me will help
 
Hello, I am looking for someone who is a doctor, or someone who knows anything about cloning. I am young reporter looking to write a full article on human cloning. I would like to know everything a doctor, or anyone here knows on the subject. I would like to know:

1) How does this technology work?
2) What are some benefits for patient care?
3) What are some ethical dilemmas this may pose
4) What are possible uses for this technology?

Anything anyone can tell me will help
You're looking to the wrong kind of doctor if you want great answers for (1). You'd want to look to a Ph.D.

For (2) and (3), use your imagination. That's not a scientific dilemma, its a dilemma that will be addressed by politicians.

For (4) just watch "The Island" with Ewan McGregor :lol:
 
Hello, I am looking for someone who is a doctor, or someone who knows anything about cloning. I am young reporter looking to write a full article on human cloning. I would like to know everything a doctor, or anyone here knows on the subject. I would like to know:

1) How does this technology work?
2) What are some benefits for patient care?
3) What are some ethical dilemmas this may pose
4) What are possible uses for this technology?

Anything anyone can tell me will help

Can't help you. Besides, you need to cite sources in your essay.
 
thank you very much, and thanks for the heads up on wiki. I know what you mean - I've found too many errors in the past. However, I always find myself coming back to it for some reason:oops:

:luck:

It wasn't an error on wiki. You just misinterpret what it said. Bacteria does have a single circular chromosome (i.e., they are haploid), and the chromosome has double stranded DNA (i.e., all "blueprint" DNA is double stranded).
 
Can someone explain to me how people get autosomal dominant diseases? I thought during inheritance we only get the gametes that our parents produce. So how does autosomal inheritance occur? I mean when a sperm cell and ovum are contacted and fertilization occurs where does the autosomal cells come from that allows this kind of disease to occur. I'm curious since I been watching a drama show, during break sessions, about this girl that contracted Spinocerebellar Ataxia which is a form of autosomnal dominant disease. I thought Lamarckian theory of evolution was false :confused:?! Thanks
 
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Can someone explain to me how people get autosomal dominant diseases? I thought during inheritance we only get the gametes that our parents produce. So how does autosomal inheritance occur? I mean when a sperm cell and ovum are contacted and fertilization occurs where does the autosomal cells come from that allows this kind of disease to occur. I'm curious since I been watching a drama show, during break sessions, about this girl that contracted Spinocerebellar Ataxia which is a form of autosomnal dominant disease.

I'm not sure about spinocerebellar ataxia in particular (I think there are several types with different population frequencies), but some genetic diseases have a high rate of denovo mutation. Neither parent carries the disease alleles, but it is present in the offspring (mutation early in embryological development). In some cases, the somatic line of the parent is normal (hence blood sample will reveal no abnormalities), but there is mutation is in the germ line. Achondroplasia for example, is an autosomal dominant disease with a rate of ~80%.

You should also consider the penetrance and expressivity of genetic diseases. Even if a person carries the disease alleles and should "theoretically" show the disease phenotype, a certain percentage of people might never show the signs of disease or might show variable degree of expression.

As a final note, dominant and recessive classifications are somewhat ambiguous. Few disease alleles are completely dominant or completely recessive. It is the nature of the defect when expressed phenotypically that results in the dominance or recessiveness. e.g., Metabolic diseases tend to be autosomal recessive, because the body can usually maintain normal function with a reduced level of particular enzyme. Only when there is complete absence will there be problems. e.g., Many inherited forms of cancers are said to follow an autosomal dominant inheritance pattern although they are actually recessive. Try and figure this one out.

I thought Lamarckian theory of evolution was false :confused:?! Thanks
I don't think anybody would ever want spinocerebellar ataxia. The "want" is an essential element of Lamarck's theory.
 
thanks a lot

but I am baffled as to why its called autosomal "recess/domin" disease when in reality its a mutation disease that occurs during the embryo stage? The way its called it makes it seem like the autosomes from the parents are inherited.
 
thanks a lot

but I am baffled as to why its called autosomal "recess/domin" disease when in reality its a mutation disease that occurs during the embryo stage? The way its called it makes it seem like the autosomes from the parents are inherited.

But the child who has the genetic disease will be able to pass it on.
 
I think this is wrong here

When Clacium binds troponin in muscle cells, the binding site for which of the following is exposed?
A) tropomyosin
B) Myosin
C) ATP
D) ADP
E) Pi

ok obviously the answer is A, but the freaking book I have says its B? WTC? Myosin is the larger filament that brings the high potential head and it doesn't have anything blocked its ACTIN that is blocked by troponin complex. I am right right? I hope so.
 
Ca++ binds troponin, and that moves tropomyosin, which covers the myosin binding site on the actin filament, out of the way so that the myosin head can bind to the actin fillament.

This picture explains it well. B is definitely correct. Hope that helps :)

http://www.arn.org/docs/glicksman/090104%20fig4a%20tropomyosin.jpg
 
Ca++ binds troponin, and that moves tropomyosin, which covers the myosin binding site on the actin filament, out of the way so that the myosin head can bind to the actin fillament.

This picture explains it well. B is definitely correct. Hope that helps :)

090104%20fig4a%20tropomyosin.jpg

But wouldn't that be ACTIN(the thin filament) that is being exposed? not myosin? Myosin is the thick filament that has the active head so it doesn't need to be exposed.
 
But wouldn't that be ACTIN(the thin filament) that is being exposed? not myosin? Myosin is the thick filament that has the active head so it doesn't need to be exposed.
"the binding site for which of the following is exposed"

The binding site for myosin is exposed. That binding site is on Actin.
 
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