RE: Article: Forcing Darwin's hand: capturing natural selection in a
- From: "John Edser" <edser@xxxxxxxxxx>
- Date: Sun, 21 May 2006 23:36:21 -0400 (EDT)
"Robert Karl Stonjek" rstonjek@xxxxxxxxxxxxxx
snip<
"One of our most surprising findings is that an estimated 20 million point
mutations gave rise to just six populations that were capable of vying for
dominance," said lead researcher Yousif Shamoo, associate professor of
biochemistry and cell biology. "This suggests that very few molecular
pathways are available for a specific molecular response, and it points to
the intriguing possibility of developing a system to predict the specific
mutations that pathogens will use in order to become resistant to
antibiotics."
snip for brevity<
"The duplicate study suggests that the pathways of molecular adaptation
are
reproducible and not highly variable under identical conditions," Shamoo
said.
JE:-
The above yet again verifies Waddington's Canalization/Assimilation model
provided over 50 years ago in which hidden epistatic genes code for the many
hidden developmental pathways that lead to any one phenotypes. These hidden
genes can switch a phenotype which has only been correlated to a major gene,
anyway. Waddington remains the only researcher to _quantify_ the overall
effects of these hidden genes within Haldane's single locus gene centric
model via the selective coefficient k2 thereby replacing heuristic gene
centricity with a minimal organism centric population genetics.
Empirically, evolutionary theory was and remains Darwinian fertile organism
mono-centric and not Neo Darwinian gene centric (or just chaotically
poly-centric). Total Darwinian Fitness (TDF) remains the key but it has been
deleted from all gene centric models. Only the models that I have posted
here include it.
Please refer to Waddington's model which I posted without comment in the
thread "Waddington's Revision of Haldane". Against all reason, the wall of
silence that surrounds Waddington's minimally organism centric model
persists.
Canalization:
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ui
ds=12082173&dopt=Abstract
Quote from the above:
"For example, Rutherford and Lindquist (6) recently uncovered vast genetic
variation by compromising the function of Drosophila Hsp90, a stress-induced
chaperone protein that confers stability on a variety of signal-transduction
proteins. They conclude that Hsp90 serves as an evolutionary "capacitor,"
buffering genetic and environmental variation except under extreme
conditions, at which point the expressed variation becomes available for
natural selection."
Assimilation:
http://8e.devbio.com/article.php?ch=22&id=213
Quote from above:
Most mammalian skin has the ability to form calluses on areas that are
abraded by the ground or some other surface.1 The skin cells respond to
friction by proliferating. While such examples of environmentally induced
callus formation are widespread, the ostrich is born with calluses where it
will touch the ground (Figure 1). Waddington and Schmalhausen hypothesized
that since the skin cells are already competent to be induced by friction,
they could be induced by other things as well. As ostriches evolved, a
mutation (or a particular combination of alleles) appeared that enabled the
skin cells to respond to some substance within the embryo. Waddington (1942)
wrote:
Presumably its skin, like that of other animals, would react directly to
external pressure and rubbing by becoming thicker. . This capacity to react
must itself be dependent upon genes. .It may then not be too difficult for a
gene mutation to occur which will modify some other area in the embryo in
such a way that it takes over the function of external pressure, interacting
with the skin so as to''pull the trigger' and set off the development of
callosities.
By this transfer of induction from an external inducer to an internal
inducer, a trait that had been induced by the environment became part of the
genome of the organism and could be selected. Waddington called this
phenomenon "genetic assimilation," while Schmalhausen (1949) called it
"stabilizing selection." Both scientists had used orthodox embryology and
orthodox genetics to explain phenomena that had been considered cases of
Lamarckian "inheritance of acquired characteristics."
JE:-
The heritable variation available to selection is either high or low geared.
EMPIRICAL multiplicative and therefore low gear genetic effects conserve
(canalize) heritable phenotypes OR in high gear, quickly switch them
(assimilate) so that a new phenotype becomes coded for. It is clear to me
that only heritable epistasis can account for common biological observations
where some of them have been on the table for centuries. However, the vast
majority of epistasis remains deleted within Haldane's gene centric
population genetics model which even today, dominates evolutionary theory
misrepresenting it. Not a single gene centric fitness has ever been
documented in nature, no matter how you define fitness. Please note that
meiotic drive genes are NOT an exception. I am happy to debate/expand on any
of these arguments.
Regards,
John Edser
Independent Researcher
edser@xxxxxxxxxx
.
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