Re: Genetic or Epigenetic: The Causal Basis of Evolutionary Change

On Feb 21, 8:58 pm, CNCa...@xxxxxxx wrote:
On Feb 21, 10:51 am, John Harshman <jharshman.diespam...@xxxxxxxxxxx>
wrote:



CNCa...@xxxxxxx wrote:
On Feb 19, 6:45 pm, John Harshman <jharshman.diespam...@xxxxxxxxxxx>
wrote:
CNCa...@xxxxxxx wrote:

[snip]

Well, let's start at the beginning. How about short and tall pea plants,
yellow vs. green endosperm, and wrinkled vs. smooth seed coats? (I
haven't looked up the exact reference, but it would be some time in the
1860s by some guy named Mendel.) Are they a) not genetic, b) not
morphology, or c) necessarily deleterious or neutral?

In the context of our discussion on epigenetic evolution of metazoans
this implies that you cannot bring up a single case of a change in
genes that has led to an evolutionary morphological change in the
animal world.
You know that my theory deals with  metazoans alone.

What theory? That the CNS does something that somehow gets
transmitted to gametes which somehow in turn produces CNS without any
interaction with the genome either in parent or offspring? Something
that somehow contains "information" that somehow gets transmitted from
generation to generation. And that this something somehow contains
"information" that is *never* encoded in the DNA genome, but in which
evolutionary differences between individuals is transmitted outside
the genetic system of the Central Dogma (DNA <-> RNA -> protein)? But
somehow this extra-genetic system is not merely the transmission of
environmental information (which, of course, is what the CNS does) via
feedback by gene regulation systems (aka, physiology).

And your evidence that the set point, for example, is not genetically
determined is...?

It is off the
topic to ask for an explanation of how my epigenetic neural mechanism
of evolution can axxount for the dwarf and normal phenotypes in
nerveless pea nut plants? Don't you think you are asking for a lot?  

Plant development, if anything, is often far more controlled by local
environmental cues than the development of *any* animal. If you look
at bushes that have genetically identical seeds planted side by side
by side you will find that their body morphology will differ far more
than the bodies of genetically identical animals because animal body
morphology is more rigidly determined. And, as I have repeatedly
pointed out, development in mammals is far more regulatory and not
mosaic like that of amphibians and many invertebrates. That *means*
that there is far less determination of morphology based on maternal
'factors' deposited in the oocyte of mammals than in mosaic
development organisms. Your so-called theory makes no such
distinction.

As John says, you mistake proximal phenotypic indicators and
physiologic responses to environment as if they were *necessarily*
themselves hereditary factors rather than genetically determined
states within the range of genetic responses to environmental
conditions. Genes are typically regulated, not rigidly either on or
off. There *are* genes that influence phenotypic factors such as
height and weight. Height and weight in mammals have both genetic and
environmental factors that determine any individual's specific
phenotype, including genes that affect how much of particular hormones
are produced, genes that affect basal metabolism, and regulatory
sequences in genes that determine the timing of puberty. As an
example of how *genes* affect morphology, there is a mutation in mice
called _little_ that is a mutation in the growth hormone releasing
factor receptor (GHRFR) gene. The phenotypic consequence is dwarf
mice. The mouse CNS is otherwise perfectly normal and capable. A
transgene of a rat GH linked to promoter sequences that activate *any*
gene downstream when the organism is exposed to heavy metals was
introduced to these mice (in 1982, this being old knowledge). Now,
when the gene is activated by heavy metals (not the CNS, which
produces GHRF) one gets giant mice. That is, the "set point" of mean
weight, all other environmental features being equal, is the precise
nature of these genes (the only thing that has been changed). And it
is the transmission of these genetic changes (not your imaginary CNS
factors from the parent) that determines the set point of the
offspring. So here we have *three* heritable phenotypes (dwarf,
normal mouse, giant mouse) where the *heritable* feature is clearly
the presence or absence of particular DNA genes.

Now what, do you think, determines the set point for the critical
weight in moths?

I
have never seen you accept the burden of proof for your statements.

To the above, I could literally add thousands of DNA-based Mendelian
factors in many organisms that affect various phenotypes, be they
behavioral, morphological, or physiological (all other things being
equal). Even most of the phenotypes you call "epigenetic" are
ultimately due to specific genes (and their DNA-based regulation).
And *heritable differences* in phenotype almost always are ultimately
DNA-based differences in sequence (if not in the coding sequence, in
the regulatory sequence).

Except for some events that are due to chance or are probabilistic
(such as prion-like switches or the choice of which X chromosome to
condense), *most* epigenetic phenomena that have been studied in
detail are *genetically* regulated and the *capacity* to produce the
epigenetic effect is *genetically* transmitted (as with maternal
effect genes), with specific gene mutations that can alter the effect.
You have made major claims against that without any evidence that I
can see. Only discussions of proximate phenotypic effects that can be
altered by environmental conditions.

Most gene regulation is at the transcriptional level. Even regulation
past the transcriptional level has genetic roots. Essentially almost
*any* phenotype that is dependent on DNA, RNA, or protein sequence is
*at base* going to be genetically transmitted. You have not ruled out
genetic transmission by pointing out that genes are regulated.

The other big thing you ignore is Weissman's concept that the soma is
the gamete's way of producing more gametes. Changes that die with the
soma are NOT themselves transmitted to the next generation. Only
features that are present or transmitted to the gametes are
transmitted to the next generation. There is a lot of evidence that
the major source of information transmitted to the next generation is
DNA-based genetic information. Excluding maternal effect factors
(particularly in organisms with mosaic development), very little
epigenetic information (rather than the genetic capacity to engage in
epigenetic phenomena) is transmitted between generations. Most that
is is labile and does not persist more than a few generations, and
that largely in unicellular organisms.

[snip]

.

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