molecular genetic proof against random mutation (1)

[QUOTE]Originally posted by peter borger:There can only be two reasons for not responding to my question:1) You do not know the content of your refernces,
2) You do not understand the content of your references.If this is the case, do not hesitate to ask.[/B][/QUOTE]Peter, I have to say that after reading a number of your posts and the associated references that I think that you are the person who either does not know the content or meaning of your own references. While I have not had the chance to get the references that SLPx was citing the abstracts appear to support his position far more than yours. And this would not be the first time that your statements were in direct opposition to the references that you cite, ie Ascorbic acid in a debate on the ID section of this board.
EvC Forum: evidence that intelligent design can't explain------------------
"Chance favors the prepared mind." L. Pasteur
Taz

quote:

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Originally posted by peter borger:

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So what I claimed was:
"the third step in vit c synthesis already yields vitamin C by spontenaous oxidation." The amounts are sufficient to prevent scurvy!

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Therefore the GLO gene --which does the fourth and final step in vit C synthesis-- is redundant!!!!!

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Reference: http//yarchive.net/med/vitamin_c.html

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Best Wishes,
Peter

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Peter, I missed this one in a reply to you other post but it is germane to my post. This is WRONG!. Please see my referenced post for the correct sequence for the synthesis for ascorbic acid. While the final step is spontaneous GLO is required for the step prior to the spontaneous one. In other words, the gene is not redundent. If you do not believe me please see the synthetic pathway that I provided for you.Opps, sorry I just noticed that the original synthetic pathway was missing. Here is a different copy
The Natural History of Ascorbic Acid in the Evolution of the Mammals
I will try to find the other one as it was far more complete from a biochemical point of view. However, please note that step 4 is GLO, while the sponteous step occurs farther down the biosynthetic pathway only AFTER GLO performs it required function. So you are still wrong
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"Chance favors the prepared mind." L. Pasteur
Taz[This message has been edited by Dr_Tazimus_maximus, 08-22-2002][This message has been edited by Dr_Tazimus_maximus, 08-22-2002]

quote:

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Originally posted by peter borger:
dear Tazimus,

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Thanks for your mail. I will check it out.
However, --according to my information-- cessation of biosynthesis in humans can result from two different gene defects. Firstly, through inactivation of the GLO gene that specifies an enzyme that converts the final step that involves an enzyme (step 4 in your reference). Secondly, trough a defect in the lactonase gene, that specifies a gene that converts the 3rd step in your reference.
The lactonase defect prevents any vitamin C synthesis at all, while the defect in the GLO gene still yields measurable amounts of vit C, because the substrate will spontaneously decompose to 2-keto-gulono-gamma-lactone in the presence of oxygen (this step in normally carried out by GLO gene product). The final step is a spontaneaous conversion to vit C (Thus, there are two spontaneous steps in the presence of oxygen). So, the only difference --if you don't express the GLO gene-- is speed of production. If one has an active lactonase gene spontaneous Vit C productions are around 15-20 mg/day. Sufficient levels to prevent scurvy.

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Best wishes,
Peter

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Peter, I just reviewed the structures and I think that you are in error. The only other step that I can see which is likely to have any significant rate of occurance at all in the absence of enzyme would be the formation of the lactone ring from the corresponding acid. This is a common reaction with sugars. THe GLO reaction with the resulting oxidation of the alchohol to the ketone is not likely ro occur without the help of the enzyme. The only reason that the final reaction occurs spontaneously is the assistance of the resonance structure accross the C-C bond and the two oxygens. Please site the source that tells you otherwise so I can look at it.------------------
"Chance favors the prepared mind." L. Pasteur
Taz

[QUOTE]Originally posted by peter borger:
A careful look at the structures in your reference demonstrates an OH group that can be oxydize spontaneously yielding a double bonded O group. This is sufficient to yield the endproduct in low concentration. I found this information in a communication between Dr. S. Harris and Dr. M. Banschbach on the internet.
QUOTEPeter, first that kind of oxidation into a more stable ketone generally does not happen spontaneously but rather requires acidic conditions and/or the presence of certian metals or other electron carrying materials, chromium is a common one in the organic lab, that can act in the reaction.I found the location of your citation on the web and, unfortunately, there is no included citation concerning the lack of activity of gluconolactonase. The value of 10 to 15 mg a day cited is actually the level that the liver releases at when the patient is near biochemical scurvy and this release can go on at this rate for quite a while, ie a couple of months, depending on the storage levels in the liver. Some of that info was in one of the papers by Levine et al. (the one in PNAS) that I incuded in my earlier post. I have done a number of searches on the web today, on both common and more medically based systems, and can not find ANYTHING on a gluconolactonase mutation in humans or other primates. The only other area that even mentioned something like this was one concerning eskimos and ascorbic acid. The problem there is that raw fish can contain ascorbate and so do certian varieties of seaweed. So much for them as examples of humans with no ascorbate requirements. I found nothing on Sub-saharan tribes as mentioned in your citation. Now, as to the sea voyages. People DO store ascorbate to different degrees, the same is true about the consumption. However, other than that one unsubstantiated comment by your citation, I can find nothing to support humans that do not require ascorbic acid. I am going to be able to hit a much larger database on Monday, it essentially has links to anything ever published that can relate to biology or chemistry so I will let you know then.Now, all of this aside, what does this have to do with the wonderful molecular correlation of the GLO pseudogene (actually non-functional gene product would be a better term) with the predictions of descent with modification? Sorry, while I do want to complete this aspect of ascorbate biosynthesis it is getting a little off track.

quote:

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Originally posted by Philip:
Dear Taz,

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A) Regarding one's quest for proving random mutation, i.e., in mutation spots,

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While I'm amazed at Peter's tenacity to disprove random mutation in certain theorized mutational spots (if you will in my meager understanding), it makes empirical sense to me. For how can the mutation spot possibly be random when it must be determined? Else random mutations (if they were indeed random) would almost always invite detrimental mutations more than beneficial ones (eg. 999 to 1 or whatever). Thus the whole concept of random mutations is a misnomer for determined ones at mutation spots.

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How deterministic vs random are these mutation spots, really Taz?

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Hi Philip, first I think that we need to review a few definitions concerning deterministic, causal and random. Here is Merriam-Websters
"1 a : a theory or doctrine that acts of the will, occurrences in nature, or social or psychological phenomena are causally determined by preceding events or natural laws b : a belief in predestination
2 : the quality or state of being determined"
Now, please note that a deterministic occurance can be a part of natural laws WITHOUT being either predestined or controlled by an outside force. So, using the standard definition based on natural lawa mutations can be both deterministic (based on natural laws) and random (based on the fact that these changes are non-predetermined or not controlled by an outside force at a site within the genome). while I will agree that mutations are not 100% random, as there are differences in the odds of having a type of mutation at different sites the term as used by most biologists is accurate based on the definitions above. As to the beneficial vs harmful, first most are neutral or near neutral as far as we can determine. Second, a neutral or near-neutral mutation can become either beneficial or harful depending on changes environmental circumstances.

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B) Who and how could one assert an organism's consistently occurring gene is non-functional: Are you asking us to believe:
1) We empirically know it has no function whatsoever,
2) That it does not and/or will not react with protein factors, genes, and/or harmones.
3) That its presence is totally arbitrary and expendable in the grand scheme (if you will) of the organism's posterity.
4) That it doesn't even serve as a functional gene-molecule for nucleotide connectivity or other functions.

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Your question is quite broad. My answer is that it depends on exactly what you are talking about. A sequence of DNA which has a known function can be defined. An alteration with a known effect can be defined. In this case GLO is a known gene and there is a known mutation that renders the protein-gene product non-functional w.r.t. ascorbic acid biosynthesis. The same mutation in the same gene in most other primates has the same effect, namely a nutritional requirement for ascorbic acid. This same gene, when not mutated allows for the biosynthesis of ascorbic acid. (As an aside to Peter, I have gone through the lit search that I mentioned on Friday and can find NO mention of the mutation that your citation mentioned, nowhere in ANY biological, chemical, or medical literature in the largest database in the world. I used pretty broad search criteria as well. I think that both you and your citation are in error w.r.t. scurvy, GLO and gluconolactonase). Now, if humans and other primates were not related would we expect to see the same mutation in the same gene, I rather doubt it.

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In sum, I don't see molecular genetic proof against beneficial random mutation as even necessary to prove that mutation spots must be determined. Such relational determinants must exist (in part at least) to enhance beneficial mutation.

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Again, beneficial random mutation seems a contradiction in terms, regardless of mutation spot characteristics; better phrased I might state them perhaps as: beneficial deterministic mutation.

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My heralding "beneficial deterministic mutation" does not imply complete non-randomization events occurring at the gene level; please don't misunderstand me. I only imply that detrimental mutations are the only truly random mutations.

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Is it that black and white, really; I think so.

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The only way that your statement would make sense would be if we lived in a universe that operated under the principles of Aristotle, namely that everything is only a represenation of an ideal. This form of determinism is not born out by ANY of evidence. There is no real data to support that certian mutations are predetermined to make an enzyme "better" at what it is supposed to do. At its simplest, a mutation changes the expression of an amino acid or of several amino acids in a protein. This changes the function of the protein in some way. That protein either provides a better or a worse interaction with the environment. It really is that simple in its conception, and that powerful in its full application.------------------
"Chance favors the prepared mind." L. Pasteur
Taz

quote:

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Originally posted by Mister Pamboli:
[B][QUOTE]At its simplest, a mutation changes the expression of an amino acid or of several amino acids in a protein. This changes the function of the protein in some way. That protein either provides a better or a worse interaction with the environment. It really is that simple in its conception, and that powerful in its full application.[/B][/QUOTE]

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Actually, it is even simpler and more powerful. The protein does not provide a better or worse interaction, merely a different interaction. It is the qualitative directionlessness of the mutation that gives the system its remarkable suppleness: the "quality" of the mutation, and any inference of intentionality in the mutating process is nothing more than a post factum ascription of value-based terms as a shorthand for the selective process.

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Yes, I was trying to put it in terms more relevant to Philip's statements to make a point ie. beneficial or harmful. Actually mutations may also act in a neutral or near-neutral fashion w.r.t. the protein activity.------------------
"Chance favors the prepared mind." L. Pasteur
Taz

Hi Peter,

quote:

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Originally posted by peter borger:
Still you did not provide evidence against Dr. banschbach claim that I refered to. So, let's wait and see.

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Actually I had put in an aside to you in reply #112 of this thread. After an extensive search by a friend of mine who essentially has access to pretty much the entire biological/biochemical/medical database I could find no mention of any mutation within the human genome of the gluconolactonase gene, either systemic or tissue specific. This is important as the protein is not only involved in ascorbate biosynthesis but is also involved in a number of other sugar pathways. Here is a brief overview of the protein
Ask.com - What's Your Question? n%2Fredirurl%2Efcg%3Furl%3Dhttp%3A%2F%2Fwww%2Echem%2Eqmul%2Eac%2Euk%2Fiubmb%2Fenzyme%2FEC3%2F0101a%2Ehtml%26qry%3Dgluconolactonase%2Band%2Bhuman%26rnk%3D1%26cz%3De07e52f691c53fea%2 6src%3DDH%5FASK%5FSRCH%26uid%3D01e08afb2a45f87d3%26sid%3D19a30bfb2a45f87d3%26u%3D&ac=24&adcat=jeev&pt=EC+3%2E1%2E1%2E1%2D3%2E1%2E1%2E50&dm=http%3A%2F%2Fwww%2Echem%2 Eqmul%2Eac%2Euk%2Fiubmb%2Fenzyme%2FEC3%2F0101a%2Ehtml&io=0&qid=8DDDA753E604214A842D67F3D1A2A12A&back=ask%3Dgluconolactonase%2BAND%2Bhuman%26o%3D0%26qsrc%3D0%26meta%3D1% 26IMAGE1%2Ex%3D7%26IMAGE1%2Ey%3D11&ask=gluconolactonase+AND+human&dt=020906113544&amt=
and
SIB Swiss Institute of Bioinformatics | Expasy
Now, every single reference that either I or my friend could find (Sorry, I can not give you links to her search, due to firewall constraints she had to send me text copy and damn was it long ) indicated that the mutation in man was in the GLO gene and NOT in the gluconolactonase gene. The site that you indicted did not provide ANY support for the mutation of the gulonolactonase gene. Every paper that I can track down says otherwise. Even in groups which were originally thought to be able to synthesize ascorbate (Eskimos)it turns out get ALL of it in their diet. One thing that I find suspicious in the sites statements is that the level of poduction that indicted in the site is almost exactly the same as the level at which the liver releases stored ascorbate (again, I refer you to the paper that I posted for you earlier in PNAS by Levine et al. where they performed the first ascorbate bioavailability study). As I mentioned earlier the oxidation event to produce 2-dehydrogulonolcatone is not going to proceed to any appreciable extent under physiological conditions. It requires acidic conditions and generally an electron carrier (Steitwiesser and Heathcock, Organic Chemistry). The only reason that the reaction with 2-dehydrogulonolactone to 2,3-dehydrogulonolcatone occurs is the partial resonance structure accross the double carbon bond of carbons 2 and 3 with the carbonyls on the same carbons. In short, I have found no data anywhere to support either your or his contentions that GLO is not the sole mutatant in the ascorbate biosynthetic pathway in humans and a great deal of data contrary to your statements. [quote][bold]
"I didn't use the redundancy of the GLO gene to support non-random mutation, since I have better examples of that. What I did was block of the pseudogene argument of evolutionists by demonstrating that the sequence of the inactivated GLO gene does not change at random. I already pointed it out to Mark24. So, if an unknown molecular mechanism generates the mutations one can never use this gene to demonstrate common descent. In fact, one cannot use any shared sequence anymore. I expect the same for shared retroviruses, but it would need a careful scruteny of 'all' known sequences (as demonstrated for the 1G5 gene in Drosophila). It would invalidate the evolutionists' strongest argument for common descent. That's what the fuss is about."[/b][/quote]That is what I thought. Well the paper that everyone was quoting earlier indicated that, with the exception of the mutation shared between most primates which inactivates the GLO gene, the remaining mutations were random. In fact, the paper that you were discussing earlier Ohta + Nishikimi BBA 1999 states (and I did point this out earlier) that,
"The 164-nucleotide sequence of exon X of the gene was compared among human, chimpanzee, orangutan, and macaque, and it was found that nucleotide substitutions had occurred at random throughout the sequence with a single nucleotide deletion, indicating that the primate L-gulono-gamma-lactone oxidase genes are a typical example of pseudogene."
So with the exception of ONE shared deletion mutation, the remainder of the mutations are random as would be expected in genetic drift found in a pseudo-gene.Sorry, I have to say that I find your arguements in this area to be very contrary to the evidence.One aside concerning the possibility (completely unshown to date, but if you can provide some supporting data or references, and not just a Q+A site, please do) of humans who make their own ascorbic acid. There is a paper that points out, rightly, that there could be undiscovered pathways dealing with the secondary metabolic fluxes
L-ascorbic acid biosynthesis - PubMed
While the data does not support your earlier assertions that does not mean that they are impossible; it just means that there is no data in support of them yet. However, for this one instance, the existence of a shared secondary pathway would not indicate that descent with modification was not supported. That would a least require (in the case of humans) a completely different metabolic system appeared in some humans that had no analog or possible original use in either other populations of humans or in closely related primates. The appearence of such a pathway in a geologically young species (important point here Tranquility) with no indication of a precursor or analogous pathway could be interpreted as a creation event. The shared GLO pseudogene with one mutation stopping the production of the gene product along with the RANDOM mutation demonstrated by the available evidence indicates common descent.------------------
"Chance favors the prepared mind." L. Pasteur
Taz

Hi Peter,

quote:

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Originally posted by peter borger:
Still you did not provide evidence against Dr. banschbach claim that I refered to. So, let's wait and see.

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Actually I had put in an aside to you in reply #112 of this thread. After an extensive search by a friend of mine who essentially has access to pretty much the entire biological/biochemical/medical database I could find no mention of any mutation within the human genome of the gluconolactonase gene, either systemic or tissue specific. This is important as the protein is not only involved in ascorbate biosynthesis but is also involved in a number of other sugar pathways. Here is a brief overview of the protein
Chemistry - Queen Mary University of London
and
SIB Swiss Institute of Bioinformatics | Expasy
Now, every single reference that either I or my friend could find (Sorry, I can not give you links to her search, due to firewall constraints she had to send me text copy and damn was it long ) indicated that the mutation in man was in the GLO gene and NOT in the gluconolactonase gene. The site that you indicted did not provide ANY support for the mutation of the gulonolactonase gene. Every paper that I can track down says otherwise. Even groups which were originally thought o be able to synthesize ascorbate (Eskimos) it turns out get ALL of it in their diet. One thing that I find suspicious in the sites statements is that the level of poduction that indicted in the site is almost exactly the same as the level at which the liver releases stored ascorbate (again, I refer you to the paper that I posted for you earlier in PANS by Levine et al. where they performed the first ascorbate bioavailability study). As I mentioned earlier the oxidation event to produce 2-dehydrogulonolcatone is not going to proceed to any appreciable extent under physiological conditions. It requires acidic conditions and generally an electron carrier (Steitwiesser and Heathcock, Organic Chemistry). The only reason that the reaction with 2-dehydrogulonolactone to 2,3-dehydrogulonolcatone occurs is the partial resonance structure accross the double carbon bond of carbons 2 and 3 with the carbonyls on the same carbons. In short, I have found no data anywhere to support either your or his contentions that GLO is not the sole mutatant in the ascorbate biosynthetic pathway in humans and a great deal of data contrary to your statements. [quote][bold]
"I didn't use the redundancy of the GLO gene to support non-random mutation, since I have better examples of that. What I did was block of the pseudogene argument of evolutionists by demonstrating that the sequence of the inactivated GLO gene does not change at random. I already pointed it out to Mark24. So, if an unknown molecular mechanism generates the mutations one can never use this gene to demonstrate common descent. In fact, one cannot use any shared sequence anymore. I expect the same for shared retroviruses, but it would need a careful scruteny of 'all' known sequences (as demonstrated for the 1G5 gene in Drosophila). It would invalidate the evolutionists' strongest argument for common descent. That's what the fuss is about."[/b][/quote]That is what I thought. Well the paper that everyone was quoting earlier indicated that, with the exception of the mutation shared between most primates which inactivates the GLO gene, the remaining mutations were random. In fact, in the paper that you were discussing earlier Ohta + Nishikimi BBA 1999 states (and I did point this out earlier)
"The 164-nucleotide sequence of exon X of the gene was compared among human, chimpanzee, orangutan, and macaque, and it was found that nucleotide substitutions had occurred at random throughout the sequence with a single nucleotide deletion, indicating that the primate L-gulono-gamma-lactone oxidase genes are a typical example of pseudogene."
So with the exception of ONE shared deletion mutation, the remainder of the mutations are random as would be expected in genetic drift found in a pseudo-gene.Sorry, I have to say that I find your arguements in this area to be very contrary to the evidence.One aside concerning the possibility (completely unshown to date) of humans who make their own ascorbic acid. There is a paper that points out, rightly, that there could be undiscovered pathways dealing with the secondary metabolic fluxes
L-ascorbic acid biosynthesis - PubMed
While the data does not support your earlier assertions that does not mean that they are impossible, it just means that there is no data in support of them yet. However, for this one instance, the existence of a shared secondary pathway would not indicate that descent with modification was not supported. Unless a completely different metabolic system appeared in some humans that had no analog or possible original use in either other populations of humans or primates. The appearence of such a pathway in a geologically young species (important point here Tranquility) with no indication of a precursor or analogous pathway could be interpreted as a creation event. The shared GLO pseudogene with one mutation stopping the production of the gene product along with the RANDOM mutation demonstrated by the available evidence indicates common descent.------------------
"Chance favors the prepared mind." L. Pasteur
Taz[This message has been edited by Dr_Tazimus_maximus, 09-10-2002]

quote:

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Originally posted by peter borger:
Dear Taz,
Thanks for your scrutiny. I will send a mail to Dr. Banchbach were he got his information.

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I would be interested in seeing any references concerning scurvy and its causes that implicate a gene product other than GLO.As to your other statements, I need to look at the paper again. There is one strain of rats which also has a GLO mutation (a group of Wistar rats if I remember correctly) which makes the homozygotes susceptable to scurvy. I will try to find that paper as well.------------------
"Chance favors the prepared mind." L. Pasteur
Taz

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Originally posted by peter borger:
I have some additional remarks/comments. You say that vit c is stored in the liver. As a oxygen radical scavenger I wondered whether the reduced form of vit c can be stored that long.

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Yes it can.

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In general, if oxygen is present it is expected that vit c is oxydized. So, storage of vit c in the liver should be under anaerobic conditions, or in the presence of strong reducing agents. Isn't it?

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Most intracellular environments are reducing. THat is one reason why, during protein purification, biochemists often add reducing agenst such as DTT in vitro, it helps to keep reduced thiols in proteins reduced. There are also a number of reducing systems that ensure that ascorbate remains reduced, the main one being reduced glutathione. There are a number of papers by Levine, Mark A. et al. that describe this system and its relationship to ascorbic acid.

quote:

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Furthermore, I got my email back from Dr Banschbach --undeliverable, wrong address-- so I will try to find it out another way.

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That would be good because all of my sources indicate that he is in error. I still have not made it to the library to get the original of the GLO mutation paper, I hope to get there next week.------------------
"Chance favors the prepared mind." L. Pasteur
Taz

Hi Peter, the largest problem with your statements concerning mutation and randomness appear to me to be a confusion with respect to: 1) randomness with an equal probability of a specific occurance over the range of possibilities, 2) randomness with a non-equal proability of a specific occurance over a range of possibilities, 3) and a non-random occurance of a specific possibility over a range. I am sure that there is a better statistical means of saying this, my stats are self taught although sufficient to compile, analyze and submit clinical and production data through the FDA. NDS deals with the second, not the first as you seem to be indicating. In fact, every reference that you have pointed out supports this treatment of the results far more than number 3 (your apparent approach). The Science paper on Histones, which I had on hand, is very supportive of this interpretation as well. The higher rate of mutations in actively transcribing genes has been well known for years. The fact that both the primary and secondary structure of genes play a role in the probability of a mutational event at those sites is also well known. The mutational frequency that everyone talks about is an average of the much higher probability sites and the much lower probability sites. Your directed mutation seems to me to be nothing more than the increased probability based on structural features and is therefor not in conflict with NDS at all.------------------
"Chance favors the prepared mind." L. Pasteur
Taz

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Originally posted by wj:
I am curious as to whether the GLO pseudogene issue, previously mentioned on this thread, was ever resolved.

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Is there any evidence that humans synthesise ascorbic acid, either through spontaneous oxidation (message #101) or some undiscovered pathway? Is there any evidence of a population of vitamin C synthesisers such as nomads or eskimos?

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I have been able to find no evidence to back up PB's claims (Peter, I am using PB to differentiate you from the other pro-evolution Peter, hope that you do not mind). Peters "source" for the two fold mutation was a comment by a person claiming to be a researcher posting onto a medical questions board. He essentially claimed that 1) there was also a mutation in a lactonase based activity gene and 2) that the reaction which glo performed occured at low rates in situ. I have been unable to find ANY data suporting assertion number one in any of the medical, biological or biochemical publications and I have associates with access to the most wide ranging databases in the world. I think that assertion number two is in error as the oxidation/reduction event required for the generation of the same intermediate as the GLO gene synthesises occurs under more stringent conditions than are generally found in vivo, namely strong acids and a metallic catalyst (info from Strietweiser, Organic Chemistry). The second oxidation/reduction event which actually produces ascorbic acid is spontaneous but it is helped along by its position next to the first and by a resulting partial resonance structure. Finally, the rate of production cited by PB's source is actually the release rate by the liver in dietery scurvy conditions. As to the eskimoes and nomads, the only data that I found dealt with eskimo's and it was discovered that, beofre their diets changed, they ate a lot of raw fish which was rich in ascorbic acid. So much for a sub-population which made ascorbic acid.

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In Peter Borger's scenario of directed (by environmental factors) mutations, wouldn't deprivation of dietary vitamin C be a significant directing environmental factor? If only a single mutation is required to convert the GLO pseudogene back to a functional GLO gene and prevent scurvy, why hasn't this mutation been witnessed in dietary stressed humans?

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If the vitamin was not present in the diet (a level of 200 - 400 mg/day is easily achieved) then yes, it would be a stresor. As to the mutations, I believe that there have been subsequent, non-shared, mutations in the glo gene since the first primate mutational event long ago. I have been unable to get to the NIH to get the paper so I do not have sequence data here. The final answer is that I do not think that there is data in eukaryotes to support PB's directed mutagenesis claims, in any genes.------------------
"Chance favors the prepared mind." L. Pasteur
Taz

quote:

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Originally posted by peter borger:

Are neutral positions in the DNA expected to change faster over time?

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If yes, please explain.
If no, please explain.

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Best wishes,
Peter

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Peter, I want to change your question slightly so that there is no confusion, ie faster with respect to what. In other words you can not compare mutations rates between areas which are condensed differently, nor can you compare mutational rates between hot and non-hot spots which derive their higher mutational rates from sequence differences or expression level differences. With that in mind, it is my understanding that sites which code for functions which are not under positive selection can accumulate changes faster than sites which are under selection in areas of the genome which are physically similar w.r.t. basal mutation rates. There are two reasons, the first is a simple one, natural selection against deleterious phenotypes; the second depends on the gene product, some proteins are less able to tolerate mutations while maintaining their function (histones come to mind). Genomic sequences under these constraints should (if I remember the concepts correctly) have fewer fixed mutations within a population than sequences with similar physical structures but without these selectional constraints.Now, I would like to direct you to post 163 of this thread. Can you please reply to my question/statement there.------------------
"Chance favors the prepared mind." L. Pasteur
Taz

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Originally posted by peter borger:
Furthermore 0.026 and 0.033 is both 0.03. So what's your point w.r.t common descent?

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Not really, it very much depends on the number of significant digits. Many academics forget about the (pardon the pun) significance of sig. digs.Been without sleep or rest for too long. Bed time.------------------
"Chance favors the prepared mind." L. Pasteur
Taz

[QUOTE]Originally posted by SLPx:
Looks pretty random to me - even within species (see Ptr1 and 2, Pan troglodytes).Of course, the 'non-random' distributions are what we call synapomorphies.[/B][/QUOTE]I thought that synapomorphies dealt more with phenotypic traits than genotypic traits. Is this a recent use of the term. I have to admit that I am behind on the changes in molecular biology terms as my current work is much more into physical biochem and biochem engineering as they relate to the production and definition of biopharm products than I am into the straight molecular bio. By the way, thanks for the reference earlier.------------------
"Chance favors the prepared mind." L. Pasteur
Taz