molecular genetic proof against random mutation (1)

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Originally posted by Percipient:
What'd I say, what'd I say!! (so I can remember for next time - )

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--Percy

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Percy, it may be that you had the temerity to ask for clarification on PB's sttatements and offer alternative possible explanations which did not involve the complete falsification and overthrow of NDT. I hope you will not be so skeptical when PB publishes his discovery in a peer-reviewed scientific journal....sometime.In the meantime, are we to be treated to the sight of Fred Williams and Tranquility Base arguing over random or directed mutations on biblical grounds?BTW, is "random mutation" considered to be:
1) random with respect to any type of mutation (duplication, deletion, substitution etc.) occuring at any point in a genome with equal probability;
2) mutations occuring in the genome which are random in regard to the fitness of the resulting genotype;
3) both, or;
4) random with respect to some other criterion?

[QUOTE]Originally posted by SLPx:Better yet, since it is your claim that 'non-random mutations' exist and falsify NDT, and that this 'information' is pre-existing in the genome, maybe you can present some genetic analyses that demonstrate that some gene that is needed for survival but is not active exists in multicellular eukaryotes (provide the sequence of the genome), expose this multicellular eukaryote to some stressor, then demonstrate that the gene needed - and only the gene needed (i.e., not genome wide) is activated via a specific mutation.Syrely you can do this, since you claim to have falsified NDT.Your simplistic defintion of 'random' seems awfully out of place.[/B][/QUOTE]Wouldn't the GLO pseudogene be a prime candidate for such a demonstration? There is strong evidence that it would be a fully functional gene with a few correcting mutations. Individuals can be stressed by removing dietary sources of vitamin C.Where is the evidence that such protein directed mutations have occurred? Are these only mutations within somatic cells or do they also occur in gamete cells?BTW, where is the evidence that members of nomadic tribes have functional GLO genes?

I am curious as to whether the GLO pseudogene issue, previously mentioned on this thread, was ever resolved.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?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?

Peter Borger, could we see your interpretation of the human and primate GLO pseudogenes using your directed mutation hypothesis.

Peter Borger, do you have any response to messages 167 and 168?

Let me ask one fundamental question which I don't recall being asked before.How does one distinguish between random and non-random mutations in Brorger's scenario of directed mutation? Is a mutational "hot spot" necessarily a non0random mutation and also a directed mutation?

PB, any answer to my question at #249?