Posted by:
Dobry
at Wed Aug 17 16:42:15 2011 [ Email Message ] [ Show All Posts by Dobry ]
What I am saying is there is NO evidence that is the case. As Kerby has pointed out he has done the breeding experiments and shown that the darker individuals are clearly expressing a single mutant allele that happens to be recessive.
I have also done these experiments THIS YEAR, so I have SOME limited data on this subject.
What I am saying, (my hypothesis) and I do intend to prove this out, is that the striped aberrant is one allele, hypermelanism is another allele, hypomelanism is yet another allele, the black belly is probably also an independent allele. (THEY COULD BE DIFFERENT MUTATIONS WITHIN THE SAME GENE, but that does not really change the explanation or the experiments to prove it so)
You are looking at this from a population perspective, and I am looking at this from an individual genetic perspective.
If said individual does not appear darker, it is not expressing the hypermelanism trait. HOWEVER.......That does not mean, that individual does not carry the trait to pass on to future generations. Perhaps the hets do have a different look, they are still not expressing the darker pigment.
Maybe the hets have some type of survival advantage, and that keeps the recessive mutation's presence at a high percentage within the population, because in every litter there is a percentage that are hypermelanistic.
You cannot say, just by looking at several individuals within a population, that clearly have phenotypic differences, that they are all variants of a specific gene just because of where they are found. There is NO evidence of that.
It is like saying that a southern accent is genetic because everyone that lives in the south talks funny, but that the gene has much variation because it can be found in almost everyone that lives there.
However, from breeding experiments that I and others have done before me have shown, that the darker phase is regulated by a single recessive mutation.
I predict that you could isolate the aberrant gene and produce litters with 100% aberrant individuals without the darker appearance and vice versa. Same with hypomelanism, black bellies and the like.
While I am not saying that your observations are wrong, I am saying that there is an explanation that can be tested with carefully planned breeding experiments, and what you will see is the variation you see for the Eiseni "locality" is regulated by the independent expression of several genes OR different mutations within the same gene. The fact that several of these traits are commonly found in the same snake, and locality suggests that this cluster of genes (or multiple mutations within a gene) are often inherited together.
However the fact that they can also be isolated from eachother clearly shows that they are independent mutations/phenoypes.
If someone can show otherwise with breeding experiments I will stand corrected, but at this point all the evidence points to the simple recessive allele explanation. ----- "We are challenging the soft bigotry of low expectations" George W.
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