Re: 50% mutation

From: r norman (rsn__at__comcast.net)
Date: 02/22/05 

Date: Tue, 22 Feb 2005 13:27:23 -0500 (EST)

On Tue, 22 Feb 2005 01:25:12 -0500 (EST), br.hessels@planet.nl
(A.C.H.) wrote:

>r norman <rsn_@_comcast.net> wrote in message news:<cvbsnn$14gf$1@darwin.ediacara.org>...
>> On Sun, 20 Feb 2005 16:41:30 -0500 (EST), br.hessels@planet.nl
>> (A.C.H.) wrote:
>>
>> >A lot of evolution is the result of quantitive changes. In human
>> >evolution, for example, more brain, less hair, less snout etc. etc.
>> >
>> >These changes are the result of changes in the regulation of genes;
>> >how much, when and where a certain gene-product is produced. (And not
>> >of changes in the gene-products themselves.)
>> >
>> >The thing i want to point out is that the variables more-less,
>> >earlier-later are one-dimensional. A mutation in a regulatory sequence
>> >results in a phenotypic change along one dimension.
>> >
>> >Now consider a situation of directional selection, a situation where
>> >some adaptive change is required.
>> >
>> >The chance of a favorable mutation, a mutation with with positive
>> >fitness, is exactly 50%. (since either more or less, earlier or later
>> >necessarily results in positive fitness.)
>> >
>> >Am i missing something?
>
>
>> You are missing a lot of things.
>
>i admit i'm not exactly hindred by a fine knowledge of biochemmistry.
>
>
>> A mutation in a regulatory sequence can make the regulation totally
>> non-functional. Speeding it or slowing it are not the only
>> possibilities.
>
>
>I'm sure that mutation can be seen as damage, creating hopeless
>monsters.
>On the other hand I suspect that mutation can be seen as something
>more controlled. Mutation, though random in relation to fitness,
>non-random in the sense that it adds variation of a certain magnitude,
>in particular regions of the genome.
>
>It is important to consider the origin of mutation in relation to
>Natural selection.
>Small mutations are not selected against, because the new alleles will
>have a fitnesses very close to the original alleles. The smaller the
>phenotypic effect of a mutation the weaker it will be selected
>against.
>This also has the consequence that mechanisms that allow for small
>mutations will not be selected against. Mechanisms that allow
>mutations to happen in a controlled way, in certain regions of the
>genome, will evolve.
>
>
>> The timing and magnitude of a regulatory process has little linear or
>> even direct relationship to the nucleotide sequence of the regulatory
>> site.
>
>
>I was thinking about something like this:
>"Molecular origins of rapid and continuous morphological evolution"
>http://www.pnas.org/cgi/content/abstract/101/52/18058
>
>In this case tandem repeat expansions and contractions are directly
>linked to the snout-length of dogs.
>
>Given some directional selection, either a repeat more, or a repeat
>less, must necessarily result in positive selection. The chance of a
>positive (as well as negative) mutation is 50%.
>
>Perhaps this way of regulating gene-expression is an example of an
>evolved mechanism that allows for the controlled addition of variation
>in the genome.
>
>
>
>> Even if what you say is true, it is quite possible that the timing
>> involves a critical zone or a critical magnitude so that both more and
>> less, or earlier and later are detrimental.
>
>
>See above. Thanks for the reply. Your clear and terminable posts in
>this group are appreciated.

Thanks for the comment.

I didn't mean to suggest that your proposal was unworkable or
impossible, only that it was unlikely. Most mutations would not have
the effect you describe but where there is a continuous effect of some
mutation, like repeat count, on phenotype and where directional (as
opposed to stabilizing) selection acts, then you are quite correct.

I hadn't seen that recent Fondon and Garner paper you cite. They
"offer a hypothesis that gene-associated tandem repeat expansions and
contractions are a major source of phenotypic variation in evolution."
On the other hand, their data comes from dog breeds, animals highly
selected through extremely severe artificial selection specifically
for particular morphological features. So such a situation might be
quite unnatural. It is more likely that nature would quickly drive
such a selective system to an "optimal" point so that mutation in
either direction would be detrimental. I was also thinking more of
the Huntington Disease situation where CAG repeat counts greater than
36 indicates disease but the time course or severity of the disease
does not seem closely related to the actual repeat count value.

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