Again, I would like to thank
Michael for posting this article
to sbe.

Michael Ragland wrote:

> Published online before print July 30, 2002, 10.1073/pnas.172388999
> PNAS | August 6, 2002 | vol. 99 | no. 16 | 10229-10230
> Commentary
> Progress on canalization
> Stephen C. Stearns *
> Department of Ecology and Evolutionary Biology, Yale University, New
> Haven, CT 06520-8106

> Stearns Article:
> In the 19th century, when evolutionary biologists focused on whole
> organisms, development played a central role in evolutionary theory. For
> much of the 20th century, genetic models and explanations replaced
> development at the center of evolutionary thought. Connections to
> development resurfaced at mid-century (1, 2) and accelerated after 1975,
> fueled by influential books (3–5) and by a resurgence of interest in
> the role of phenotypes in evolution and in the tension between recent
> selection and historical  constraint in the design of organisms.

JE:-
It has ALWAYS been the case that selection
can only operate on the phenotype. The refocus
of selection to the genotype was ALWAYS just a
misused population genetics over simplified
model allowing a non refutable theory of
nature. Such gross misuse continues to this very day
and is justified using Post Modern epistemology
(the school of thought that suggests everything
is relative). What has been discarded is the Popperian
process of refutation allowing political bigotry
to dictate what the science of biology is.
The net result is that creationist have climbed
onto the same bandwagon forcing "creation science"
to be taught to innocent children in some schools
in the USA in the name of science. The damage caused
by model misuse is enormous. The Neo Darwinists
that post here refuse to address this issue.

> Stearns Article:
> By the
> turn of the new  millennium, development had again become a major
> evolutionary theme in two quite different but interestingly connected
> ways. Under the label of Evo–Devo, the tools of molecular genetics are
> used to explore deeply conserved developmental mechanisms that are
> active early in development and thought to shape the regulatory systems
> responsible for the conservation of basic body plans (6). Under the
> label of the Genotype–Phenotype Map, a variety of theoretical and
> experimental programs explore the mechanisms and processes that shape
> the expression of genetic variation in phenotypes in nonlinear ways (7).
> Is there a natural bridge between these two research fields? Do the
> deeply conserved developmental systems that produce adult morphology
> also influence the expression of genetic variation in the traits they
> shape? Such a connection would point to part of one of evolution's
> long-sought Rosetta Stones: the mechanisms connecting macro- to
> microevolution. Building on work by A. Wagner (8), Siegal and Bergman
> (9) provide one of the first demonstrations of the plausibility of such
> a connection for a major component of the genotype–phenotype map:
> canalization.
> Canalization, now a classic idea, was suggested independently by
> Waddington (1) and Schmalhausen (2).

JE:-
To my knowledge only Waddington altered
Haldane's basic population genetics equations
to include a new variable: "developed in X".
Professor Felsenstein (who amazingly
was a student of Waddington can provide
the reference to any interested sbe reader).
This added variable allowed for genetic
epistasis (non additive gene associated
information) to now be included in just a
basic way. Fisher deleted it entirely.
Later genetic epistasis was redefined to only
mean "additive genetic information". This
term was just a gerrymander to get around the
fact that Fisher had deleted genetic epistasis
entirely because additive genetic epistasis
is only the equivalent of zero epistasis.

Sadly, Waddington's revision remains entirely
ignored to this very day. The reason this is
so is to preserve the myth that genomic genes
can be _independently_ and not just
_dependently_ selected opening the
door for organism fitness altruism (OFA) using
Hamilton et al logic. However, apart from
the fact that an independent gene level of
selection does not even exist within nature
(this fitness level was always just a misused
heuristic model) Hamilton's rule remains
in error by the value m. OFM can only be
proven when rb-c > m whereas Hamilton
et al incorrectly insist it can be proven
when rb-c > 0 (please refer to posted articles
on this subject). The Neo Darwinists that post
here refuse to discuss such a correction.

> Stearns Article:
> Schmalhausen argued that
> canalization resulted from stabilizing selection shaping developmental
> mechanisms to buffer the expression of traits, holding them near their
> optimal states despite genetic and environmental perturbations.
> Waddington suggested that if canalizing mechanisms could be disrupted,
> hidden genetic variation would be released. He claimed to have perturbed
> canalizing mechanisms with environmental treatments of developing fruit
> fly larvae and from the increased genetic variation in the treatments
> inferred the existence of canalization. Recently, Rutherford and
> Lindquist (10) for Drosophila and Quietsch et al. (11) for Arabidopsis
> (Fig. 1) have demonstrated that altering development with inhibitors of
> HSP 90 causes a release of hidden genetic variation. This has attracted
> great interest, for if the inference of canalization from the evidence
> of released genetic variation is correct, then at least one very
> concrete mechanism causing  canalization would now be within sight.

JE:-
The above work provides "on the face of it" evidence
for the heritability of non additive genetic information
(genetic epistasis). The tiny size of the Human genome
(making a mockery of Haldane's dilemma) also provides
the same evidence. What this means is that as far as
heritability is concerned a form of population genetics
"dark matter" (in astronomy most of the mass of the
universe is hidden away as dark matter)  must exist that
provides the vast majority of heritable information.


> Stearns Article:
> However, the logical basis of that inference is not yet firm for several
> reasons. Waddington and Schmalhausen's original formulation of
> canalization has been remarkably difficult to define precisely in modern
> terms.

JE:-
This is because a non additive genetic code does not exist
as yet. Such a code must exist if genetic epistasis constitutes
heritable information.

> Stearns Article:
> Gibson and G. Wagner (12) express the essence of one problem:
> canalization describes a reduction in the expression of variation in
> phenotypes relative to some standard, but what standard?

JE:-
The supposed Fisherian standard of additive effects.
Assimilation increases the expression of variation in
phenotypes, i.e. canalization and assimilation represent
a multiplicative gearing mechanism for expressed variation.
The problem is gene centric Neo Darwinism cannot even separate
variation from evolution because of their consistent misuse
of over simplified models. They define evolution as:
any gene frequency change in a deme. This definition allows
heritable random changes via just a random process to be able
to cause  evolution in their own right. Random processes such
as mutation and sampling error (so called genetic drift)
cannot cause evolution in their own right. The gene
frequency changes they cause only constitute variation and
not evolution. I have proposed an experiment to test
this proposition (but only to non verification because
allowing any random process to cause evolution in its
own right remains irrefutable so it is not a scientific
proposition, anyway). Because gene centric Neo Darwinism cannot
even separate variation from evolution what hope do they
have attempting to understand how genetic epistasis may be
coded?


> Stearns Article:
> It has been
> difficult to control all of the effects that are plausibly involved to
> isolate a clear signal that could only have been produced by canalizing
> mechanisms. Another not entirely unrelated issue is that of unexplored
> alternatives: does the experimental release of hidden genetic variation
> necessarily demonstrate canalization because that is the only
> alternative, or is it simply consistent with canalization, leaving open
> plausible alternatives not yet eliminated? If so, what are those
> alternatives?

JE:-
Can anybody here provide any testable alternatives?
If not does this mean that canalization and assimilation
as hypothesis for heritable epistatic information can just
be ignored? Why has Waddington's revision of Haldane's
basic population genetics equation been ignored for so
long?

> Stearns Article:
> We now have a short but growing list of plausible alternative
> hypotheses that have not been rejected for mechanisms that reduce
> phenotypic variation and, when perturbed, release hidden genetic
> variation. These mechanisms do not necessarily have much to do with the
> original scenario for the evolution of canalization; they produce the
> appearance of canalization as a byproduct of other processes. Siegal and
> Bergman (9) describe one such mechanism. Because they build on an
> approach taken by A. Wagner (8), let us first consider his main result.
> A. Wagner defined a phenotype as a state of gene activation and modeled
> evolution as changes in the strength of regulatory interactions among
> the genes. The elements of his model correspond to cis-acting
> transcription factors and to the genes whose  expression they regulate.
> A. Wagner demonstrated that such regulatory networks acquire higher
> genetic robustness—better genetic canalization—under stabilizing
> selection. Similar results have since been found by several others. So
> far, so good: modern insights appear to be consistent with classical
> concepts.
> Then a problem surfaced with the selection scenario thought to produce
> genetic canalization. Suppose that canalization evolves to buffer the
> phenotype against genetic perturbations caused by mutations. G. Wagner
> et al. (13) showed that the strength of selection for canalization
> increases with three variables: the intensity of stabilizing selection,
> the degree of canalization caused by the modifying allele, and the
> amount of genetic variation affected by the canalizing effect. However,
> at mutation–selection balance, the amount of genetic variation
> available for such a canalizing gene to work on will be reduced as the
> strength of stabilizing selection increases, for in eliminating genetic
> variation, stabilizing selection "eliminates the effects for which
> canalizing alleles are selected... Only with high mutation rates can
> genetic canalization be effectively  selected in mutation-selection
> balance" (14). Because such high mutation rates (>10–4 per locus) do
> not seem  generally plausible, neither does the evolution of genetic
> canalization as a mechanism to buffer against the disruptive effects of
> mutations. If that is the case, then how do we account for the dramatic
> release of hidden genetic variation, now well anchored as an
> experimental result?
> One possibility, the answer that Siegal and Bergman propose, is that
> phenotypic robustness to genetic perturbation has been wrongly
> interpreted as adaptive canalization. They assume selection against
> lethals, in their context genes that do not settle on a stable gene
> expression. Such selection evolves robustness against not only lethal
> mutations but also, as an unselected byproduct, against mutations of
> smaller effect that produce quantitative variation. It does so by
> causing networks of interacting transcriptional regulators to increase
> in complexity. Thus, more highly connected networks may be more
> canalized not because canalization of quantitative variation has been
> selected but because complexity in the underlying developmental network
> has been selected to suppress the effects of lethal disruptions of gene
> expression. Canalization is then a byproduct, and the release of hidden
> genetic variation is caused not by disruption of adaptive buffering
> mechanisms that evolved to conceal the genetic variation that is
> released, but by reduction in the complexity of regulatory networks that
> evolved to prevent the expression of lethal mutants.

JE:-
It does not matter if complexity can produce canalisation
without selection, or not. What matters is what is heritable.
If genetic epistasis produces heritable
information but canalization was initially only a
mechanical side effect of complexity then selection can
now operate on this information because it is heritable.
Either Fisher's deletion of epistasis as "heritable" and thus
"selectable" information was true or false. This issue
has to met head on. At the moment is just evaded
via the misnomer: "additive genetic epistasis".

>snip<

Regards,

John Edser
Independent Researcher

PO Box 266
Church Pt
NSW 2105
Australia

edser{at}tpg.com.au
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