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  #1  
Old 05-31-2008, 01:41 PM
BigRedBeta BigRedBeta is offline
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If the DNA sequence in humans is so close to that of chimpanzees, why do the two species look so different?"
You're very correct in the issue of differences of gene promotion.

Sequence is only one part of the equation. The ways in which an individual gene is turned on - in terms of frequency, timing, and so forth - accounts for a great deal of the variety. Further, because genes have effects on other genes down the line, turning them on and off in particular sequences (accomplished through a variety of promoter and inhibitor sequences in front and behind a particular gene), matters as well.

Think of it this way. Say you have a number of red, blue and green legos. For one building, you start out with 50 red pieces, 20 blue pieces, and 30 green pieces. No matter what you build, from a color stand point, it's going to look MUCH different than the thing you build with 10 red pieces, 75 blue pieces and 15 green pieces. DNA in the fact that it essentially codes for those building blocks (proteins) is very similar.

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Well, if chimps and humans are so close in DNA and chromosome number, what if we were to use the science of In vitro fertilization. Would something come from it?
Would likely depend on what's encoded on that extra set of chromosomes, and how well a fertilization would respond to that missing set of information. As far as humans go, monosomies are poorly, poorly tolerated and result uniformly in spontaneous abortion of the pregnancy. There are only three human Trisomies (having three of a particular set of chromosome) that result in a fetus compatible with extra-uterine life - 13 http://en.wikipedia.org/wiki/Patau_syndrome ; 18 - http://en.wikipedia.org/wiki/Edward%27s_Syndrome ; and 21 - which is Down's syndrome. Edwards and Patau syndrome infants rarely live past a year. And yet, obviously Down's syndrome has a pretty variable prognosis and many individuals live long, fulfilling lives. So it's difficult to predict exactly what you're cross breeding experiment would beget.
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Old 06-01-2008, 01:49 AM
Leslie Anne Leslie Anne is offline
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Originally Posted by BigRedBeta View Post
Would likely depend on what's encoded on that extra set of chromosomes, and how well a fertilization would respond to that missing set of information. As far as humans go, monosomies are poorly, poorly tolerated and result uniformly in spontaneous abortion of the pregnancy. There are only three human Trisomies (having three of a particular set of chromosome) that result in a fetus compatible with extra-uterine life - 13 http://en.wikipedia.org/wiki/Patau_syndrome ; 18 - http://en.wikipedia.org/wiki/Edward%27s_Syndrome ; and 21 - which is Down's syndrome. Edwards and Patau syndrome infants rarely live past a year. And yet, obviously Down's syndrome has a pretty variable prognosis and many individuals live long, fulfilling lives. So it's difficult to predict exactly what you're cross breeding experiment would beget.
I'm finding this fascinating. You'll have to bear with me as I'm woefully ignorant in the sciences. (I did look up "trisomies" and "monosomies" though.) What I'm now wondering is why it would be so difficult to predict a cross breeding. If you match up like chromosomes between two different species wouldn't you at least know what wouldn't match up and result in monosomies?

(Hmm, as I'm writing this it's occuring to me why it would be difficult to predict.) I'm guessing that certain monosomies and trisomies would result in things we've never seen before?

What about with just in vitro fertilization of a human embryo into another primate?

Sorry for the silly questions. I'm just very curious.
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Old 06-01-2008, 01:56 AM
cheerfulgreek cheerfulgreek is offline
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Originally Posted by BigRedBeta View Post
Would likely depend on what's encoded on that extra set of chromosomes, and how well a fertilization would respond to that missing set of information.
So do you think the body would just reject it? That's what I was thinking.
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  #4  
Old 06-01-2008, 09:28 AM
BigRedBeta BigRedBeta is offline
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So do you think the body would just reject it? That's what I was thinking.
It's not that the mother's body rejects it, it's that the having either extra information (an extra chromosome hanging out) or missing information (having only one chromosome when you should have two) results in a non-viable fetus. This would be due to having too much or too little of needed protein or some other form of imbalance that affects the growth and development.

I base this off the fact that, in humans, there are no known viable complete autosomal monosomies (Cri du Chat syndrome is a partial monosomy of chromosome 5) and only the three previously mentioned trisomies. Just because we never see individuals with monosomies or trisomies other than the ones mentioned absolutely does not mean they don't occur, but rather, that they are completely non-compatible with even advanced intra-uterine age, let alone extra-uterine viability.

Further, in humans, more than 80% of all conceptions never make it to term, and roughly 50% of all conceptions have some sort of chromosomal anomaly that makes the pregnancy non-viable. It doesn't even necessarily have to be gross chromosomal abnormalities, as significant micro-deletions of chromosomes in the right places can create a non-viable pregnancy. Most often the pregnancy is spontaneously aborted within the first 4-6 weeks and so the woman doesn't even realize she's pregnant. (Not to open a can of worms, but these facts are one of my biggest arguments against the "life begins at conception" crowd).
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  #5  
Old 06-02-2008, 03:01 PM
cheerfulgreek cheerfulgreek is offline
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Originally Posted by BigRedBeta View Post
It's not that the mother's body rejects it, it's that the having either extra information (an extra chromosome hanging out) or missing information (having only one chromosome when you should have two) results in a non-viable fetus. This would be due to having too much or too little of needed protein or some other form of imbalance that affects the growth and development.

I base this off the fact that, in humans, there are no known viable complete autosomal monosomies (Cri du Chat syndrome is a partial monosomy of chromosome 5) and only the three previously mentioned trisomies. Just because we never see individuals with monosomies or trisomies other than the ones mentioned absolutely does not mean they don't occur, but rather, that they are completely non-compatible with even advanced intra-uterine age, let alone extra-uterine viability.

Further, in humans, more than 80% of all conceptions never make it to term, and roughly 50% of all conceptions have some sort of chromosomal anomaly that makes the pregnancy non-viable. It doesn't even necessarily have to be gross chromosomal abnormalities, as significant micro-deletions of chromosomes in the right places can create a non-viable pregnancy. Most often the pregnancy is spontaneously aborted within the first 4-6 weeks and so the woman doesn't even realize she's pregnant. (Not to open a can of worms, but these facts are one of my biggest arguments against the "life begins at conception" crowd).
Thanks for this.
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  #6  
Old 06-02-2008, 10:12 PM
AKA_Monet AKA_Monet is offline
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Originally Posted by BigRedBeta View Post
It's not that the mother's body rejects it, it's that the having either extra information (an extra chromosome hanging out) or missing information (having only one chromosome when you should have two) results in a non-viable fetus. This would be due to having too much or too little of needed protein or some other form of imbalance that affects the growth and development.

I base this off the fact that, in humans, there are no known viable complete autosomal monosomies (Cri du Chat syndrome is a partial monosomy of chromosome 5) and only the three previously mentioned trisomies. Just because we never see individuals with monosomies or trisomies other than the ones mentioned absolutely does not mean they don't occur, but rather, that they are completely non-compatible with even advanced intra-uterine age, let alone extra-uterine viability.

Further, in humans, more than 80% of all conceptions never make it to term, and roughly 50% of all conceptions have some sort of chromosomal anomaly that makes the pregnancy non-viable. It doesn't even necessarily have to be gross chromosomal abnormalities, as significant micro-deletions of chromosomes in the right places can create a non-viable pregnancy. Most often the pregnancy is spontaneously aborted within the first 4-6 weeks and so the woman doesn't even realize she's pregnant. (Not to open a can of worms, but these facts are one of my biggest arguments against the "life begins at conception" crowd).
So what are the physicians calling the Turner's Syndrome and the Philadelphia chromosome in Fragile X these days?

Just asking because I haven't kept up with that research.

Cheerful

The fertilized eggs are hypermethylated and the heterochromatin is wacky causing inappropriate crossovers and non-homologous end joining in the chromosomes.

Remember human eggs are EXTREMELY fragile unlike say mouse. Knockout/trangenics are rather difficult to do even with similar non-human primate species. And OLAW rules will NOT allow researchers to use chimps for molecular studies. The highest we researchers can get these days are baboons. But since NIH eliminated our budgets, doubtful anyone can pay for it... Even med and vet schools are are having difficulties with the animals they use for teaching...
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  #7  
Old 06-02-2008, 11:15 PM
BigRedBeta BigRedBeta is offline
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Originally Posted by AKA_Monet View Post
So what are the physicians calling the Turner's Syndrome and the Philadelphia chromosome in Fragile X these days?

Just asking because I haven't kept up with that research.
Just to make it clear - I said there are no "autosomal monosomies" - which leaves your Turner's out of the picture.

The Philadelphia chromosome (I'm not sure what you're getting at with it's relation to Fragile X - I've never heard of any association, which doesn't mean it's not out there) as a balanced translocation technically wouldn't fit the general idea of monosomies or trisomies as all the information is there (nor are there extra copies), just in an abnormal configuration...

As for the expanding tri-nucleotide repeats in Fragile X (CAG, right?)...as far as I'm aware it's a non-coding region.
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  #8  
Old 06-03-2008, 12:54 PM
cheerfulgreek cheerfulgreek is offline
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Originally Posted by AKA_Monet View Post
Cheerful

The fertilized eggs are hypermethylated and the heterochromatin is wacky causing inappropriate crossovers and non-homologous end joining in the chromosomes.

Remember human eggs are EXTREMELY fragile unlike say mouse. Knockout/trangenics are rather difficult to do even with similar non-human primate species. And OLAW rules will NOT allow researchers to use chimps for molecular studies. The highest we researchers can get these days are baboons. But since NIH eliminated our budgets, doubtful anyone can pay for it... Even med and vet schools are are having difficulties with the animals they use for teaching...
Well, I know that OLAW does a lot of the monitoring and keeps everything compliant, but aren't there other alternatives? What about PGD? I know it requires in vitro fertilization and all, but with it, through research, wouldn't scientist be able to actually do genetic tests on cells and DNA removed from an embryo, and then return the embryo to the womb?
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Last edited by cheerfulgreek; 06-03-2008 at 12:56 PM.
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  #9  
Old 06-01-2008, 01:12 AM
TexasWSP TexasWSP is offline
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Hahahahahahahaha, oh wow....now you're doing the "I'm very calm.......you're the upset one" technique . Yes, you're right. Clearly by my posts I am just seething mad. Yes, Devil Woman, it was a joke.

Did you just scold me about posting in threads? Please take a second and remove yourself from the golden pedestal you have perched yourself on . Maybe you're right though......I'm sure there's just a plethora of people on this greek life interweb message board that could write books on primate genetics.

......yes, you're exactly right.....and can read to boot. I most certainly did call you "Ms. I have a bitchy attitude".

Between your responses here and your bashing and making fun of unfortunate Subway Sandwich Artists, I felt the moniker was warranted.

You need to lighten up.

Last edited by TexasWSP; 06-01-2008 at 01:15 AM.
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  #10  
Old 06-01-2008, 02:01 AM
cheerfulgreek cheerfulgreek is offline
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Yes, Devil Woman, it was a joke.
So now I'm a devil woman....nice.
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  #11  
Old 06-01-2008, 02:04 AM
Leslie Anne Leslie Anne is offline
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So now I'm a devil woman....nice.
Don't worry about it, cheerful. Consider the source.
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  #12  
Old 06-01-2008, 02:20 AM
cheerfulgreek cheerfulgreek is offline
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Don't worry about it, cheerful. Consider the source.
Thanks for that.
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  #13  
Old 06-01-2008, 02:34 AM
TexasWSP TexasWSP is offline
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So now I'm a devil woman....nice.
Yes, you are a devil woman.

It's from Billy Madison....a movie. "Don't tell me my business devil woman......."???

Ring any bells?? Guess not. You probably don't like comedies.....they require a sense of humor. You probably hate dogs and children too....and fast food employees, haha.

Consider the source? Pffft.

Last edited by TexasWSP; 06-01-2008 at 02:43 AM.
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  #14  
Old 06-01-2008, 02:56 AM
cheerfulgreek cheerfulgreek is offline
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Yes, you are a devil woman.

It's from Billy Madison....a movie. "Don't tell me my business devil woman......."???

Ring any bells?? Guess not. You probably don't like comedies.....they require a sense of humor. You probably hate dogs and children too....and fast food employees, haha.

Consider the source? Pffft.


uhmmm...okaaay?
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  #15  
Old 06-01-2008, 01:53 AM
PhiGam PhiGam is offline
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Usually when something is produced with less chromosomes than its parents it has significant defects- I would think that Mules are a rare exception to this. The hybrid would have to have alterations on all 23 chromosome pairs- an alteration on one usually results in a severe disorder. I would guess that the offspring would be unable to develop or survive.
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