Re: Genetic or Epigenetic: The Causal Basis of Evolutionary Change
- From: hersheyh <hersheyhv@xxxxxxxxx>
- Date: Fri, 20 Feb 2009 16:42:29 -0800 (PST)
On Feb 20, 3:14 pm, CNCa...@xxxxxxx wrote:
On Feb 20, 12:10 am, hersheyh <hershe...@xxxxxxxxx> wrote:
On Feb 19, 5:52 pm, CNCa...@xxxxxxx wrote:
Despite unspecified claims made here in TO on the existence of genetic
models of evolutionary change,
*All* models of evolutionary change require *hereditary* transmission
of information between generations, whether that *hereditary*
transmission is DNA-based in the genome, DNA-based in plastids,
transmitted as an RNA-based genome, transmitted as a prion-like
crystal formation, transmitted as differential modification of the
genome (such as methylation), or transmitted as materials generated by
genomic-based maternal effect genes. The few examples of epigenetic
transmission of information across generation have the property of
"lability", often essentially resetting or changing each generation.
Moreover, what happens in the soma of multicellular organisms is
irrelevant *unless* you can demonstrate that that can *also* be
transmitted through the gametes.
more than one century of genetic
research has failed to provide a single case of a change in a gene/
regulatory sequence that has led to anything but deleterious or at
best neutral changes in animal phenotypes.
Every ignorant creationist always keeps claiming that *all* mutations
are deleterious (or, if a tad more intelligent, they might include
neutral). The *fact* is that mutations are not *inherently* anything
but a difference. The adjectives "deleterious", "neutral", or
"beneficial" are not inherent properties of a mutation. They are a
*subsequent* determination of the *effect* the *difference* has under
a defined environmental *condition*. That is the use of those terms
is *conditional* and depends on the particular environment. The very
same *difference* or *mutation* can be "beneficial", "neutral", or
"detrimental" depending on the environment the organism finds itself
in.
The *reason* why most new mutations are neutral or deleterious is
simply because the *environment* that the organism has evolved within
has already optimized the genome. The conditions under which a new
variation is likely to be beneficial is one in which the environment
has changed from the conditions of the organism's ancestors.
It would be better to be concrete than engage in explanations on the
nature of gene mutations, which hardly anyone here in TO needs.
You apparently do need such an explanation. After all, *you* are the
one claiming that there is not "a single case of a change in a gene/
regulatory sequence that has led to anything but deleterious or at
best neutral changes." That means that you apparently think that
there can be no such thing as a beneficial change in *any*
environment. That would certainly imply that you think that *any*
change in a genome must be either detrimental or neutral *regardless*
of the environment. That is, you think that the qualifying adjective
of "deleterious" (or "neutral" -- be glad I consider you in the group
of slightly more intelligent individuals who are creationists wrt your
capacity to understand) are *inherent* to any change.
The HbC allele causes resistance to malaria when homozygous. It also
causes a mild anemia. Thus the "benefit" or "detriment" of HbC is
dependent upon the presence or absence of malaria. In areas where
malaria is endemic, the "benefit" of malaria resistance outweighs the
"detriment" of mild anemia. So is the HbC 'detrimental' or
'beneficial'?
There are frequency dependent alleles. For example, self-sterility
alleles in plants. A plant that mutates to generate a new or novel
self-sterility allele in a particular area is at a strong selective
advantage, since its pollen can fertilize the ova (and its ova can be
fertilized by the pollen) *any* other plant of this species,
increasing its reproductive success relative to the plants with the
most common self-sterility allele in the area. Then, over time of
course, this allele becomes more frequent and starts having trouble
(relatively, because there are, not surprisingly, often as many as 200
different alleles of this gene) finding a plant it can fertilize
with. The new self-sterility allele is 'beneficial' relative to the
current population. Then it becomes 'neutral'. Or it may be
'deleterious', depending on the frequency of other alleles in the
population.
Strep resistance in bacteria is due to a mutation in a particular
ribosomal protein (a single aa change). The mutation also causes the
ribosomes to work more slowly, thus slowing the growth of the
bacteria. In an environment lacking streptomycin, the mutation is
"deleterious" because the bacteria having it are outgrown by the
bacteria lacking the mutation. In an environment having streptomycin,
however, the mutation is "beneficial" since it permits the bacteria to
continue to grow while the non-mutants die. So is this mutation
"deleterious" or "beneficial"? By the metric of benefit (which is
always and consistently relative reproductive success) that
determination is conditional.
Even loss of function mutations can sometimes be beneficial. Loss of
the ability to make a particular product which can also be gotten by
scavenging can sometimes lead to resistance to a toxic analog that
must be converted to the proximal toxin by a synthesis enzyme.
Although *some* neotenous salamanders become neotenous by their
failure to produce thyroxin, others have become neotenous by loss of
their thyroxin receptor. The former type can be artificially induced
to metamorphize by adding thyroxin (and some will even do so in a
regulatory fashion occasionally, although more never do produce the
necessary level of thyroxin in nature). The latter cannot undergo
metamorphogenesis. The inability to metamorphize is "beneficial" in
environments where there is a constant water source but little in the
way of moist terrestrial environments. In other areas, such as
wetlands that go dry or lack insect food for part of the year, but
which has a moist forest floor, this lack of metamorphosis is not
"beneficial".
If you
have a model of how a change in DNA can produce a change in morphology
it would be worthy of letting us know.
Achondroplasia is a common form of dwarfism that is due to a change in
DNA (a single nucleotide change, incidentally). Seal-limb. There are
tons of morphological differences (including hairy ears) that are due
to single gene variants. There are more genetic traits that cannot be
attributed to specific single genes, but which exhibit strong
heritability (such as weight and height).
Since such deleterious and
neutral changes are not favored by natural selection, mutations in DNA
could not be responsible for the colossal evolution of animal world as
we see it presently.
Ever hear of population genetics? That says you are wrong.
Apparently you, like all those brain-dead creationists, think that a
mutation has an inherent property of "beneficial" or "deleterious".
That simply is not true. The only inherent feature of a mutation is
that it is different.
We lack not only empirical evidence but even
purely speculative models of how a change in the DNA could produce an
evolutionarily relevant (not deleterious) change.
Ever hear of the entire discipline of population genetics? Take a
course. This is stuff that was new 80 years ago. Read about the neo-
Darwinian synthesis sometime. Ancient history you apparently have
forgotten.
You call this an argument?
It is irritation at your incompetence in understanding basic genetics
that was new 80 years ago.
In this post of the series I will address the problem of the
epigenetic mechanism of transmission of changes to the offspring,
what was suspected that might be a “giant hole” in my theory.
Not suspected. Is.
No substance. Empty rhetoric.
For a hypothesis that claims what? That some magical form of
"information" comes from the CNS to reside in the microtubules and
centrioles of eggs and then somehow gets re-transmitted to the CNS?
With no explanation of how this would work? And that *ignores* the
obvious role of the genome in development?
Since the epigenetic mechanism of evolutionary change is derived from,
and supported by, empirical evidence, first I will make a synopsis of
part of that evidence. And since this epigenetic mechanism is
challenging the neoDarwinian mechanism of evolutionary change I will
comparatively present the neoDarwinian and epigenetic explanations of
the mechanism of evolutionary change in each particular case. I invite
anyone here in TO to correct or improve my attempts to interpret
particular evolutionary changes from the neoDarwinian point of view.
Evolution of the body size in Manduca sexta.
In the course of 30 years, or about 220 generations, this insect
evolved a 50% increase in body size and investigators came to the
conclusion that no mutational changes but changes in three epigenetic
factors: growth rate, critical weight and timing of secretion of
neurohormone PTTH “almost completely account for the evolutionary
increase in body size observed.” (D’Amico et al., 2001; Davidowitz et
al., 2003; Davidowitz et al., 2004).
Inadequate reference. This is not the first time we have pointed out
that you have not adequately referenced this claim. BTW, the mere
claim that the increase in body size is due to "growth rate, critical
weight, and timing of secretion of...PTTH" does not prove anything
about whether or not the cause of these changes were genetic (genomic)
or epigenetic. Genetic variation can certainly result in all three
factors changing. So can a change in environment (there has been, for
example, a secular non-genetic increase in human height due to better
and more nutrition, even though height is a trait with a high
heritability).
Now you are arguing not with me but with investigators, which have
excluded the genetic variation as a possible cause of the
evolutionary change in the body size of Manduca sexta. You can write
a response to Proceedings of the Royal Society.
You could give the F**KING reference correctly. Just names and dates
is inadequate and makes me think you got this reference second hand.
All I had was your word that they excluded genetic variation. I don't
trust your competence in understanding the article. *How*, exactly,
did they exclude genetic variation? The *usual* alternative to
genetic variation is not called epigenetic variation, but
environmental variation.
NeoDarwinian explanation
From a neoDarwinian view, it would be predicted that this evolutionary
change would result from a change in genes or in genetic information
in general. This prediction seems to have been rejected by the fact
that investigators found that factors not related to changes in genes,
epigenetic factors are responsible for almost all the evolutionary
incresae in the body size. No suggestion has been made that it could
be related to any change in regulatory sequences
Again, like creationists, you assume a false dichotomy. Even if it
has been shown that the secular change is not genetic, that would mean
it is not due to *any* hereditary factors *including* epigenetic
*hereditary* factors. In that case, the appropriate attribution would
be that the secular increase is due to some *environmental* factor.
See the example with human height. That is, the environmental change
leads to a change in the mean of the norm of reaction permitted within
the genetic capacities of the organism.
Do you believe that using the label creationist is a substitute for an
argument? Seems strange to be used by a scientist.
I am pointing out that your argument is like that of a creationist,
using false dichotomy as an argument.
Epigenetic explanation
Investigators have concluded that the evolutionary change is
determined by changes in the growth rate, critical weight, and timing
of secretion of neurohormone PTTH, all epigenetic changes taking place
in the brain: changes in the function of circuits timing the synthesis
of PTTH, changes in circuits that determine the set point for ending
the growth, and the neural mechanism for timing suppression of
production of IGFs (insulin-like factors) in two clusters of neurons
in the pars intercerebralis of the insect protocerebrum.
This is, at best, a claim that body weight is affected by
environmental factors. BFD. The same is true of humans. In times of
scarcity, body weight of humans can lead to truly skeletal proportions
(or absolutely whale-like). So can bulemia and anorexia, which can be
thought of as brain chemistry defects. And starvation and bulemia and
anorexia are not obviously heritable traits. But they are within the
norm of reaction of human weight, given some extreme environments.
For this to be an example of hereditary epigenetics, you have to
demonstrate that *something* is inherited by the next generation that
is not encoded in the DNA genome.
Investigators have excluded the possibility of the change being a
change within the norm of reaction determined by environment. They
have concluded that this is an evolutionary change.
How have they excluded that?
Evolution of caste polymorphism in ants
Experiments with winged and wingless castes of Pheidole morrisi have
shown that the developmental pathway for wings consists of three
switch points; the first one that determines development of queens and
workers depends on the level of maternal JH during oogenesis. The
second depends on the external stimuli (photoperiod and temperature),
to which the embryo responds by generating brain signals
(allatotropins/allatostatins) that regulate production of juvenile
hormone (JH). This second pulse determines production of (winged)
queens, whereas lack of JH pulse determines formation of worker and
soldier larvae.
The third JH pulse determines development of soldiers from worker
larvae and the lack of JH pulse determines formation of worker
larvae.
With JH pulses as determinants of caste formation one wonders what is
the cause of differential expression of JH in P. morrisi?
NeoDarwinian explanation
Since no change in the JH gene has occurred, the change in its
expression would be brought about by a change in a regulatory sequence
of this gene. But if there is a change in the regulatory sequence it
would be present in all individuals of the same brood, which is not
the case. This rejects this hypothesis and leaves no opportunity for
developing a neoDarwinian explanation of the evolution of castes in P..
morrisi (as well as in other cases of social insects).
Epigenetic explanation
What we see in the process of caste development in this insect is an
epigenetically determined change in pulses of JH determined maternally
(the first JH pulse) and induced by activity of neural circuits in
response to extrernal stimuli, via neuropeptides allatotropin and
allatostatin that stimulate and suppress secretion of JH
respectively. The process of elimination of wings by apoptosis is also
epigenetically regulated via a signal cascade that starts in insect
brain in response to external stimuli (PTTH--> Ecdysone → EcR-Usp
(Ecdysone receptor-Ultraspiracle)--> Dronc (also E93 and BR-C) → Dronc
and Drice caspase effector genes).
Genes transmit capacities not organs. We humans, for example, have,
at zygote formation and various stages of early embryonic development,
both the capacity to go down the female or the male path (both
anlagens are present).
[Snip other equally irrelevant examples where no evidence of
*inheritance* of epigenetic factors is presented. Epigenetic changes
cannot be evolutionarily relevant *unless* they are transmitted
genetically. Maternal effect genes, for example, transmit information
both epigenetically in the form of egg cytoplasmic factors *and*
genetically. But the epigenetic effect is only transmitted to the
next generation and thereafter gets reset. The genetic factors
(alleles of genes), OTOH, get transmitted for many, many, many
generations.]
You should understand people engaging in these discussions in TO know
something more than you believe.
Such as?
Regards,
N.C.
.
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