More non-random evolution

Peter Borger says: "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. Both mechanism make the gene redundant, and that was my initial claim."But, in conditions of insufficient dietary vitamin C, debility and dead can result. Therefore the gene is not redundant by any alternative genetic or biochemical processes. Therefore, why does not directed mutation correct the "stop" codon mutation and return the gene to activity in stress conditions?"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."But why is this a common hotspot in almost all of the primates but not all other mammals? Why does the same mutation occur at the "hotspot" in the primate GLO pseudogene? Are hotspots susceptible to repeated occurences of the same mutation? Why is the same common primate mutation not found throughout mammals if this is a hotspot susceptible to a particular nucleotide substitution?I'm afraid your explanation of directed mutation for primate (and human) GLO pseudogenes instead of common ancestry is flimsy.I don't think anyone will argue that all points on a gene have an equal likelihood of mutation. However you wish to extrapolate that this means that there is a directing mechanism which produces these unequal distributions of mutations. You then imply that this means an intelligent design of a multipurpose genome. But why doesn't your directing mechanism act on the multipurpose GLO genome in conditions of scurvy?

PB, your evidence for non-random, directed mutation is flimsy because the same data can be better explained by coventional evolutionary theory. The "why" questions relate to the discrepency between your "explanation" and observations.Using your non-random, directed mutation hypothesis some predictions can be made. One prediction would be that, if the common primate "stop" codon mutation in the GLO pseudogene is the result of directed, non-random mutation then the mechanism which has produced this mutation should also operate in other genomes and produce the same result. However the vast majority of mammalian genomes have not suffered lethal mutation of the GLO gene - they have functional GLO genes. Conventional evolutionary theory explains this pattern by a common ancestor for all primates - your hypothesis does not explain the pattern except by relegating it to an unknown mechanism operating identically in most primate genomes but not operating effectively in most mammals.Why not test your hyothesis and evolutionary theory on another set of data? IIRC guinea pigs and some bats also have non-functional GLO pseudogenes. Your hypothesis would predict that the common primate mutation would also be expected to occur in those other pseudogenes because there is a non-random mutation mechanism acting. Evolutionary theory would predict that the fatal mutations in the other GLO pseudogenes have occured at random and are unlikely to be the same as the common primate mutation because there is no close common ancestor of the primates, guinea pig and bats. Therefore, if the common primate mutation is found in the other groups then this would be more supportive of your hypothesis; if the common primate mutation does not occur in the other groups then this would be strong evidence against your hypothesis and consistent with evolutionary theory.PB, I fear that you are simply using a new incarnation of the god-of-the-gaps argument. We don't know precisely why certain mutations occur more frequently than other mutations therefore there is a directed mechanism which we haven't found therefore there is inteligent design of the mechanism therefore there is a creator.BTW it's WJ.