TAXACOM Digest - 7 May 1997 to 8 May 1997

Dave Williams PROFDHW at AOL.COM
Sun May 11 02:25:31 CDT 1997


In a message dated 5/9/97 6:09:30 AM, Doug Yanega wrote:

>>Actually, I think something is missing here - if the mutant alleles are not
>>identical but have similar effects, then they could NOT form homozygotes
>>(by definition) if they came together in a single individual, which was
>>what the original pop'n geneticist *explicitly* said was involved (because
>>unless they *were* identical and *could* form homozygotes, each mutation
>>would likely vanish from the population very quickly, being neutral in
>>heterozygous form).

Then, Robin Panza wrote:

>Not quite true, because of the redundancy of the genetic code (several RNA
>triplets producing the same amino acid linkup).  Several different mutations
at
>the same site could effect the same amino acid substitution.  While these
are
>not identical mutations at the level of DNA base pairs, they are
>*functionally* identical.  They can complement each other producing the same
>biochemical phenotype in "heterozygous" form.  Either or both could spread
in
>the population.
>
>However, I think the original post was about a slightly different
phenomenon,
>one that hasn't been addressed yet.  If overall mutation rate in the region
of
>a particular peptide's gene is high, it would produce many deleterious, some
>essentially neutral, and some beneficial mutations.  The higher the mutation
>rate, the more mutations occurring, and the greater the probability of the
>same beneficial one more than once.  If a mutation is truly recessive (and
>there are many degrees of and variations on dominance), it is functionally
>neutral at low frequencies, because rare recessives make even rarer
>homozygotes.  This can allow a recessive beneficial allele to remain in the
>population long enough for a second, identical or complementary mutation to
>occur.  This effectively increases the chances for a pseudohomozygote (don't
>know the word for "heterozygous but complementary"; parazygote?), exposing
the
>allele(s) to selection.

I do hate to be this stupid, but why would having two nonidentical, recessive
alleles (that is, ones that code for nonfunctional proteins) be any different
than having two identical recessive alleles? In a double recessive, a
technically homozygous condition (two nonidentical recessive alleles) would
have the same effect on the phenotype (no functional proteins) as an actual
homozygous condition consisting of two identical recessive alleles. This
brings me back to my original question: In a classical system, how do we know
that two recessive alleles are identical if any number of possible mutations
may produce nonfunctional proteins which would have the same effect
(essentially no effect in a typical case by the failure to produce the
essential protein)?

Dave Williams
Science Division
Anne Arundel Community College
Arnold, MD 21012
Vmail: 410-541-2265
Email: profdhw at aol.com




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