Re: sci.bio.evolution mailing list


dk@xxxxxxxxxxxxxxxxxxxxxxxxx (DK) wrote:-

Recent studies of developmental biology have shown that the genes
controlling phenotypic characters expressed in the early stage of
development are highly conserved and that recent evolutionary changes
have occurred primarily in the characters expressed in later stages of
development. Even the genes controlling the latter characters are
generally conserved, but there is a large component of neutral or nearly
neutral genetic variation within and between closely related species.
Phenotypic evolution occurs primarily by mutation of genes that interact
with one another in the developmental process. The enormous amount of
phenotypic diversity among different phyla or classes of organisms is a
product of accumulation of novel mutations and their conservation that
have facilitated adaptation to different environments. Novel mutations
may be incorporated into the genome by natural selection (elimination of
preexisting genotypes) or by random processes such as genetic and
genomic drift. However, once the mutations are incorporated into the
genome, they may generate developmental constraints that will affect the
future direction of phenotypic evolution. It appears that the driving
force of phenotypic evolution is mutation, and natural selection is of
secondary importance.
http://www.pnas.org/cgi/content/full/104/30/12235

JE:-
This is just back-to-the-future, stuff. The mutationists were wrong in the
past and they remain wrong, today. Chance selection (random mutation and
genetic drift) cannot compete and win against non random selection. The
problem which needs to be addressed here, i.e. not just evaded is, how can
genetics account for all the heritable differences between say, a chimp
and
a human when over 99% of the genes that code for anything at all remain
the
same in both.

Not even true. When it comes down to what matters most - proteins -
80% of them are not identical between chimps and humans.

http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubmedid=15716009

JE:-
I agree. However, I was referring to just popular, synthetic, Neo Darwinian
models and not biological reality :-) Withnin the abstact the author noted:
"the number of proteins responsible for the phenotypic differences may be
smaller since not all genes are directly responsible for phenotypic
characters." Evolution by natural selection can only concern itself with
heritable characters so Neo Darwinists simply delete genetic epistasis (non
additive gene associations) as "inherited" but not "heritable". Please note
that the main theme of my argument remains: "Chance selection (random
mutation and genetic drift) cannot compete and win against non random
selection."

What's important to remember here is that there are plenty of examples
where a single mutation in a single protein alters the way an entire cell
or
a whole organism behaves. Therefore, the 80% difference (even when
most of the difference may be restricted to a single amino acid) looks
very significant and can easily account for the difference between
species.

JE:-
Yes it is called gene fitness epistasis. It emains artificailly deleted from
every synthetic Neo Darwinistic model.

Note: both have only tiny genomes (20,000 or so coding genes).
The answer that makes the most sense to me is that NON additive genetic
epistasis accounts for _most_ of the _heritable_ variation along with
above
the gene level forms of inheritance like gene imprinting. Both remain
deleted from popular Neo Darwinian models.

The answer that makes most sense is that when a single amino acid
can alter the functioning of the whole organism and when we don't have
capacity to faithfully model this series of events, we can't possibly
have any clue as to what changes are "important" and what are not.
In other words, forgetaboutit, any attempt to account for the difference
are as reliable as attempts of predicting consequences of cold summer
in Texas on corn harvest in Iowa.

JE:-
Please tell that to Prof. Felsenstein :-)

Regards,

John Edser
Independent Researcher

edser@xxxxxxxxxxxxxx


.

Relevant Pages