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Originally posted by peter borger:
Please do not make a straw man out of the GLO gene. I mentioned several times that I do not need it to demonstrate non-random mutations.
That is true,a lthough you also mentioned that it contained directed mutations (which no one else appeared to see) so it is somewhat relevant.
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That is demonstrated in the 1G5 gene.
I should be in the NIH library Monday, I was going to go today but I did not feel like trudging through the rain carrying a stack of papers.
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In addition, it was you who introduced a putative alternative metabolic route for vit C, or a long storage capacity of vit c in the liver.
OK, I need to call you on this one. Please see your posts 101 and 105 here
EvC Forum: molecular genetic proof against random mutation (1)you were making claims that went against every single thing ever published concerning ascorbic acid metabolism, which I then pointed out to you.
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Both mechanism make the gene redundant, and that was my initial claim.
This is in error. If your claims concerning the mutation of the lactonase gene and the chemical conversion of the first hydroxyl were correct, and they do not appear to be as you have provided absolutely no suporting data while I have provided a few references that are contrary to your assertions, than yes it would be redundant. However, they are not, and if you had read the PNAS paper that I posted to you concerning the bioavailability study you would have noted that, after a long lag period where ascorbic acid stored in the liver was slowley released into the system, that thepatients suffered a precipitous drop in serum ascorbate levels indicating the onset of real scurvy. A long storage is not equivalent to a lack of requirement. GLO is not and never has been redundent. In primates it is lacking which is different.
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According to the hypothesis of 'non-random mutations and a multipurpose genome', redundant genes will be readily inactivated over time, since they are not under selective constraint. That's what we find in primates. Okay, the inactivation is in the same spot, but that may be due to non-random mutations, or if you like 'hot spot' mutations as they are called in literature.
OK, I can see one of a pair of redundent genes having more mutations due to the selective constraint, however this STILL does not point to directed mutation. It points to a filtering process. And you still do not seem to understand hot spots. There is a MASSIVE difference between an increased probability of a specific event and a directed event. Your examples appear to me (I still need to check 1G5) to be far better explained bythe former than the latter.
By the way, you did not give a source for your mutational accumulation rates concerning rat and primate GLO genes that you posted in the other thread (the one that I cited earlier). Care to share?
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"Chance favors the prepared mind." L. Pasteur
Taz
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