Re: rapid variation

GRMorton@aol.com
Fri, 8 Sep 1995 15:44:33 -0400

Nice to hear from you Walter.

You wrote:
>>Small correction. That genome size is for the human HAPLOID genome, that
is, it is the size of the genome carried by a human sperm (or an unfertilized
egg). The human offspring is diploid and receives mutations from both the
sperm and egg, thus doubling the mutation rate experienced by offspring.
Thus, by Glenn's own figures, each human progeny receives 2 x 3.5e9 x 1e-7 =
700 new mutations. <<

Some biologist might want to correct me on this but since in DNA A combines
with T and C with G, the two strings are not totally independent of each
other. I have seen some reports that there are slight differences in the
mutation rates of the sense vs antisense strings of DNA but in general it is
my understanding that a mutation in one will normally be matched in the other
during cellular division. If this is the case, then your comment about
haploid/diploid is irrelevant to the problem.

You wrote:

>>I also point out (once again) that Glenn SELECTED the MHC genes because
they have the highest number of alleles. In other words, he SELECTED those
particular genes that most favored his point of view. But MHC genes are
distinctly UNTYPICAL, they do not represent typical genes. As Steve Clark
pointed out, MHC genes -- UNLIKE MOST ALL OTHER GENES -- are subject to gene
conversion, which injects genetic variation into those genes at a much higher
rate. Glenn's assumptions about the mutation process and its rate of
occurrence DO NOT APPLY TO THE MHC GENES.<<

Walter,.
The facts are not supporting your view.
So what is wrong with citing the gene with the highest number of alleles? If
you want to find the age of a forest, you find the tree with the highest
number of tree rings. Are you suggesting that I can find the age of a forest
by finding the tree with the average or least number of tree rings? This
will come as a shock to the foresters. Similarly, I am merely trying to find
out when the most recent genetic bottleneck occurred.

I was citing the DR genes, which it turns out are not subject to gene
conversion. You cite Steve Clark. I think Steve already passed judgment on
your calculation of the rise of genetic diversity. I could point you to the
place on the archive if you have forgotten.. You must have missed his post
this morning . I am sure that you would want to correct your data accordingly
so I will cite it again for you.
Steve wrote:

>>I think that this does need some clarification. The MHC gene complex is,
well, complex. For the immune system, there are class I and class II genes
(there are also class III genes which do not appear related at all to the
function of immune cells). When discussing MHC genes and their polymorphism,
especially from an evolutionary standpoint, most people talk about the class
I genes (HLA-A,B and C). The DR genes are class II genes, of which there are
more than just the DR genes.

Class I and class II genes differ by structure, function and, therefore,
relatedness. As far as I know (but I haven't kept up with the nuances of
the field) gene conversion has only been described for class I genes,
possible because there do not appear to be any class II-type pseudogenes
linked to the complex.

I had assumed that you and Graeme (sp?) were discussing class I genes, and I
took you at your word that there are "59" total alleles (I have never counted
them all, and there may others yet to be found). I will look up the
Scientific American article and see what it has to say. I'll be gone this
weekend, so I won't be able to get back to you until early next week.<<<
end quote***************

glenn