Re: [asa] Two questions...Ayala's article

Preston: in layman's terms: Ayala right, or Ayala wrong?

David W. Opderbeck
Associate Professor of Law
Seton Hall University Law School
Gibbons Institute of Law, Science & Technology

On Wed, Feb 25, 2009 at 3:40 PM, Preston Garrison <pngarrison@att.net>wrote:

>
>> Yes, the assumption that the MHC alleles survive rather than
>> convergently re-evolve is highly dubious. After all, when you're
>> trying to generate a random DNA sequence, you only have A, G, T, and C
>> to choose from.
>>
>
> No, you also have small insertions, deletions, inversions, Alu insertions,
> etc. It is easy to see these things in the alignments between primates,
> because the genomes are so similar that alignment is usually easy.
>
> On average, there will be about 25% similarity
>> between genuinely random DNA sequences. The MHC alleles must be
>> functional, so there are some constraints makign them less than fully
>> random. It has such high mutation rates that it should be possible to
>> look at some well-documented modern genealogies and check out the
>> patterns. I don't know how well one can calculate a probable
>> bottleneck diversity given the extreme overprinting of positive
>> selection for high variation.
>>
>> Also, any one individual has multiple MHC alleles.
>>
>
> No more that 4 at any locus, although a locus might get duplicated in
> various ways, which could effectively give you more 4 versions of the same
> proteins after a while.
>
>
>> A somewhat analogous situation arose in bacterial studies. Bacteria
>> were placed with a sugar that they couldn't metabolize. Some evolved
>> the ability to use it. These bacteria were re-mutated to remove the
>> ability and put back in similar conditions. They evolved the ability
>> to use the sugar much faster than before. Lamarckian evolution?? No,
>> it turned out that the bacteria had evolved a high mutation rate,
>> thereby increasing their chances of having beneficial (or harmful or
>> neutral) mutations.
>>
>
> Just to clarify, they only evolved the new ability at a rate that could be
> detected in a laboratory sized population because they had a dormant gene
> that could be activated by a mutation or two.
>
> Many experiments show that when you take a microbial clonal population,
> divide it up and put them under all under the same new culture conditions,
> they will optimize for the new conditions in a variety of ways. There may be
> common mutations that occur in multiple cultures because they can occur at
> high rates and are strongly selected for under the new conditions, but there
> are almost always a variety of mutations that contribute to the optimization
> and only occur in one or a few of the cultures. It is naive to think that
> there is only one general set of alleles possible at each locus in the HMC,
> and that they would be regenerated faithfully over and over again.
>
> I have suggested ways to test what actually happened in the e-mail I sent
> the other day.
>
>
>> The only way to have an n=2 bottleneck is if this couple were quite
>>> special in some way or ways, and that isn't "natural".<
>>>
>>
>>
>> Or to put them fairly far back in time. Actually, this aspect in part
>> reflects population genetics, too. If you have a finite population
>> with multiple alleles of a particular gene and no further mutation,
>> after enough generations there will only be a single allele in the
>> population because individuals do not all have equal reproductive
>> success and because each allele in a parent has a probability, but not
>> a certainty, of getting into the next generation. In smaller
>> populations, it's quicker. Two chunks may have different ancestors,
>> but those two individuals have a common ancestor if you go back far
>> enough, etc.
>>
>
>
> Doesn't this ignore the possibility of selection at the population level
> for maintaining many alleles at a given locus? Having many alleles at a
> given locus of the MHC, which encodes proteins having to do with immunity,
> means that when new pathogens or new variants of existing pathogens arise,
> it is more likely that some portion of the population will be able to
> respond effectively to the pathogen. If new pathogens arise regularly, which
> they do, there is continuing pressure to maintain many alleles at these
> loci. The idea that multiple alleles must eventually be reduced to one or a
> few assumes that there is no selective pressure for maintaining a large
> number of alleles. It makes sense to me that, over the long haul, there is
> all kinds of selective pressure for the maintenance of many alleles at many
> loci of the MHC.
>
>
>
>> Certainly trying to go back far enough to have a single pair
>> physically ancestral to all modern humans runs into difficulties with
>> the fact that Gen. 4 seems to depict late Neolithic technology-about
>> 10,000 years ago or so. Not absolutely insurmountable, but difficult.
>>
>> An analogy to the more spiritual interpretation of Adam and Eve's
>> parental status is the way that Jesus is the new Adam. He isn't
>> biologically ancestral to anyone, but spiritually what He did
>> transfers out to a large number of people.
>>
>> --
>> Dr. David Campbell
>> 425 Scientific Collections
>> University of Alabama
>> "I think of my happy condition, surrounded by acres of clams"
>>
>>
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>
>
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Received on Wed Feb 25 17:14:22 2009