molecular genetic proof against random mutation (1)

[QUOTE]Originally posted by peter borger:
[B]Dear SLPx,In response to pointing out the scientific evidence for me you reply:"I don't know whethyer I admire or am disgusted by this common quality in creatinists - taking something that is clearly evidence against their position and claiming that, in reality, it supports it. Strange..."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.Best wishes,
Peter[/quote]Ah - the ever present creationist condescension.No, Pete, I know and understand. What I do not understand is how you can manipulate it to make it appear to support your claims.Wishful thinking.Oh - what questions were those?[/B][/QUOTE]

quote:

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Originally posted by peter borger:
dear Tazimus,

​

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

Dear Taz,You wrote:quote:
--------------------------------------------------------------------------------
Originally posted by peter borger:
dear Tazimus,
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.Best wishes,
Peter--------------------------------------------------------------------------------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.My response:
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.Best wishes,
Peter[This message has been edited by peter borger, 09-06-2002]

[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.

Dear Taz,A) Regarding one's quest for proving random mutation, i.e., in mutation spots,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.How deterministic vs random are these mutation spots, really Taz?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.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.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.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.Is it that black and white, really; I think so.

Sorry to butt in ...

quote:

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Originally posted by Philip:
Dear Taz,

​

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

​

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.

​

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

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I think you may be missing the subtle shift the PB has been using
in terms of randomness.Random for ToE simply means we do not know when a mutation
will occur.The existence of regions of the genome which have a higher
tendency to mutate does not make any actual mutation non-random.It just means that there may be some as yet unknown mechanism involved
when mutations do occur.DNA in the brain cells and immune cells is deliberately
re-arranged in response to dunno-what(in the brain possibly some
memory storage ... New Scientst article on it a while back) and
for immune cells in response to foreign chemicals.Perhaps it's just a hang-on from that mechanism.Doesn't necessarily mean that the mutation is deterministic though,
just governed (perhaps) and by that I mean mechanistically.

quote:

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Originally posted by Philip:

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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Again, this is problem with PB's assertions ... how can you
claim redundancy when you cannot say 100% that a sequence
has no function?Maybe there are 'data' and 'code' regions in DNA????

quote:

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Originally posted by Philip:

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.

​

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.

​

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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I think you lost me here ... or are you still using a different
variation on the term random?Any mutation could be beneficial, non-beneficial, or detrimental
it all depends on expression and how that expression interacts
with the environment surrounding the cell/organism.

quote:

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Originally posted by Philip:
Dear Taz,

​

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

​

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.

​

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.

quote:

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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.

quote:

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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.

​

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.

​

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.

​

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

[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]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.

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]

​

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

Dear Taz,Thanks for your work. And I look forward to your search on monday.Still you did not provide evidence against Dr. banschbach claim that I refered to. So, let's wait and see.You wonder:
"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."I say:
"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."Best wishes,
peter

quote:

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Originally posted by peter borger:

... 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...

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Does this mean you are suggesting that there is a mechanism
which would cause any genetic sequence at a particular locus
to become the same genetic sequence given enough time?Normally one would expect that for a mechanism (or process) to
produce the same output(s), that the initial conditions would
also have to be the same.

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.

---

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]

Dear Taz,
Thanks for your scrutiny. I will send a mail to Dr. Banchbach were he got his information.Furthermore, let's have a careful look at the presented sequences in Otha's paper. At first sight one doesn't see anything out of the ordinary and one would assume randomness of mutation. However, have a look at the sequences. From orangutan to chimp 2 aa changed, and 2 aa changed afterwards (from chimp to human). Surprisingly, the aa at position 11 (from righthand side) was two times involved in this change. That is something that I wouldn't expect by chance alone. It certainly is a hotspot and that implicates a mechanism. So, if one position does not change at random why would the others have changed at random? Maybe here a mechanism was involved too. Therefore, you cannot use this gene as proof for common descent. What I like to see now is more sequences of primates including subspecies. That would clear thing up.Furthermore, as mentioned before, it doesn't matter for the mutation rate whether or not the gene has been inactivated. If it is allowed to compare these organisms and assuming paleontological timescales to be correct, the mutation rate observed in primates is (15/163):25 = 3.6(exp)-3 = 0.36% per million years. Similarly, the muation rate if rats are included (and they have a functional GLO gene) is (26/164):50 = 0.31% per million years. So, it doesn't matter whether the gene has been inactivated or not. Another reason to be a little suspicious.Best wishes,
Peter

quote:

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Originally posted by peter borger:

That is something that I wouldn't expect by chance alone.

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This is a strange comment ... what would you expect by chance?If it's 'by chance' pretty much any possible outcome should be
expected, surely.