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

CNCabej@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:
Despite unspecified claims made here in TO on the existence of genetic
models of evolutionary change, 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.
That's because when such cases are brought up, you find excuses to deny
them.
The only example I remember you have brought up is the example of
bacterial resistance to anribiotics, which is experimentally rejected
by Adam M, Murali B, Glenn NO, Potter SS. (2008. Epigenetic
inheritance based evolution of antibiotic resistance in bacteria. BMC
Evolutionary Biology 8:52). If you have another valid example I would
be very curious to see it.
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.

Not at all. But let's explore the plants a bit more.

You know that my theory deals with metazoans alone. 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? I
have never seen you accept the burden of proof for your statements.

I knew you'd find some way to weasel out of it. So you agree that genetic differences can produce differences of morphology in plants? That's progress. Now, what fundamental difference between animals and plants makes this case invalid? What prevents animals from having the same type of genetically caused, morphological differences we see in plants?

This is off the record:
I will try to respond although I can't claim to feel comfortable with
your request. What I know, and don't expect me to present any sources
here, is that the length of these plants, as of almost all plants,
depends on circulating plant hormones, gibberellins. These hormones
are not direct products of genes but of the activity of a few enzymes,
products of a few genes.

As I have pointed out in earlier posts, even though plants have no
nervous system, they also succeed to maintain their structure during
their life time, a few days to hundreds of years. This implies that
some kind of a control system has to exist if they have to grow,
reproduce, and evolve. The metazoan nervous system is not THE control
system of the living world; it is the only control system we know in
some details, whereas the control systems in plants are less known.

The patterns of expression of genes coding for enzymes of the
gibberellin pathway, just like all the non-housekeeping genes, depend
on the needs of the growing or reproducing plant organism. Hence,
humoral signals from various parts of the growing/reproducing plant
have to somehow signal these genes for producing enzymes for
gibberellin synthesis. Plant physiologists and geneticists know that
such signals for the beginning and ending synthesis of gibberellin
enzymes come continually by a circulating hormone auxin. Experimental
prevention of the synthesis of this hormone prevents/reduces sharply
expression of gibberellin enzymes and the plant growth.
What occurs in the dwarf form of the pea nut is that a mutation(s) in
the gene(s) for gibberellin enzyme(s) prevents/downregulates
transformation of the hormone in its active length-promoting form.
Again the expression of gibberellin enzyme genes is not self-
regulatory, it is function of extracellular humoral signals, the
hormone auxin. What regulates auxin? This is where the knowledge of
the control system in plants, as opposed to that of metazoans, ends.

Yes, the dwarfism in pea nuts seems to result from a mutation in one
of genes of gibberellin pathway. If you remember, I have also
repeatedly admitted the possibility of “useful mutations” to the
extent that it was admitted by one of the founders of neoDarwinism,
Theodosius Dobzhansky, who believed that finding a useful mutation is
so hard as finding a needle in the haystack (of deleterious
mutations). I take it for granted that this is a useful mutational
change in plant morphology. What role might have such mutations
played in evolution of the plant kingdom? The jury is still out but
the exceptional scarcity of such examples is not promising.

Ah, so now you're claiming...what? That useful mutations do exist but are so rare as to be unimportant in evolution? Well, that's progress too. You had previously claimed that there was not a single case, and now you admit that there are at least a few.

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.
True iff there are no such things as advantageous mutations. Are you
really making this extremely strong claim? It seems to be a claim that
genotype has nothing to do with fitness. It's easy to show that genotype
does affect fitness, and that different genotypes have greater or lesser
comparative fitness depending on environment. It would seem that
advantageous mutations must therefore exist, unless you suppose that
these genotypes have all existed since the beginning of time.
It is not the first time I am explaining you the same thing. If not
distraction I can't guess what is your purpose. Creating a straw man?
I have made it clear here in TO that gene mutations are the source of
evolution of genes and evolution of proteins and, as I have repeatedly
told you, they are the main source of the biochemical evolution in
unicellulars and multicellulars. What I am saying, and I believe you
know it well, is that there is no evidence that would causally relate
occurrence of a gene mutation to evolution of specific change in
morphology. So far you have blatantly failed to provide any relevant
evidence. Should I hope you will in the future?
What exactly do you mean by "morphology" here, as distinguished from
"phenotype"? I'm not sure what differences count as morphological to
you, and what don't.

Not more than what J.W. von Goethe meant: visible biological
structures.

So would you agree that tall/short, green/yellow, and smooth/wrinkled are all morphological features?

At any rate, there are plenty of genetic
differences that result in morphological differences. That's pretty much
all classical genetics could detect.

John, being so demanding with others in providing evidence, you too
have to provide evidence (evidence from "classical genetics" on a
change in a gene that has led to an evolutionary change in
morphology). You have failed to do it so far. Can I expect you to do
it this time?

I believe I have just given you three. Haven't I?

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.
Now you're just getting silly.
I am not good in this kind of rhetoric but you are doing worse in
providing evidence in support of your statements. If you have an
example of a change in DNA producing a change in morphology you should
present it here. If you don't why should anyone believe you have?
Apparently all research in genetics to date has shown differences that
are evolutionarily irrelevant. Is that correct?

Not until you admit that you have not found an example. I am still
waiting for you to find an example.

Sorry, I thought you had just agreed that tall/short, at least, was such an example. Was I wrong about that?

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.
Finally! But I'm not holding my breath.
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.
No. Please. All your "evidence" so far has been irrelevant, and it just
postpones the moment of (supposed) revelation.
Again rhetoric? I don't believe you don't see the abundant evidence. What your ignoring rhetoric only suggests is that you lack the confidence to confront that evidence.
No. It suggests that I don't think your evidence has anything to do with
what you are claiming.

You are simply ignoring, not arguing against my evidence.

Not so. You have not presented any evidence to argue against. All your evidence shows is proximate pathways of development. You have not shown a single difference between species that is inherited non-genetically.

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).
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
How did investigators find this? Why are you still unable to post a
complete citation?
I would recommend you to read the original article (D'Amico et al.
2001. The developmental and physiological basis of body size evolution
in an insect. Proceedings of the Royal Society London Series
Biological Sciences 268: 1589-1593)
Thanks. That is a real citation. You need to do that consistently.

And I've read the paper. It doesn't say what you think. It talks about the evolution of developmental mechanisms, but it's clear that the authors believe those mechanisms are under genetic control. For example, the size increment between instars didn't change, and they speculate that's because of a lack of additive genetic variance for that trait. The point here is that nothing in this paper is at odds with selection of genetic variation, and the authors realize that even if you don't.

However, for your convenience here are not one but two
"complete citations"
No. Those are not citations. Those are quotes. Learn the difference.

Thank you. Good point, although off the topic.

I'm merely trying to educate you about scientific terminology, so you can respond appropriately.

1. (From the abstract) "Changes in these three developmental processes
completely account for the observed evolutionary change in body size."
Irrelevant. What caused the changes in those developmental processes? I
claim that genetic differences are at the base. You have shown no
evidence to the contrary.

There is a little but important difference between us. You make a
statement that "genetic differences are at the base" and do not feel
obligated to support it with evidence.

In this I'm in agreement with the authors of that paper you just cited. Your "evidence" isn't actually relevant to your thesis, as the cited paper shows.

I have argued adequately here
in TO:

1.Why the growth rate is epigenetically determined by neurally
expression of insulin-like genes in the CNS (ablation of these neurons
alone causes development of flies with reduced size).

Again, not relevant. You continually confuse proximate mechanism with ultimate cause. What is inherited that makes growth rates different? You haven't shown anything relevant to that question.

2. The critical body size is epigenetically determined in the brain:

"The assesment of the critical body size is made in the brain and is
based on processing of the signals sent by he insect's stretch
proprioceptive neurons that receive mechaniical stimuli of increasing
stretch as a result of increased body size" (Gorbman and Davey, 1991,
see full reference in my previous post) and

3. PTTH delay time is computated in the insect's brain in response to
photic signals.

Now, where is your evidence "that genetic differences are at the
base"?

Where is your evidence that they aren't? You haven't connected any of these epigenetic mechanisms to inheritance.

2. From conclusions:
"We can estimate the contribution of each of these factors these
factors to the final weight as follows. The 1999 growth rate after
achieving the critical weight was
ca. 2.4 g day71 whereas in 1972 it was ca. 2.1g day71. By multiplying
the growth rate by the delay time and adding
this to the critical weight, we obtain a prediction for body
size. For 1972 this prediction is 2.1g day71 Â1.5 days
( 36 h) + 5.0 g 8.15 g and for 1999 it is 2.4 g day71
 2.1days ( 50 h) + 6.0 g 11.04 g (taking the conser-
vative estimate of 6.0 g for the new critical weight). These
values are within 5% and 1%, respectively, of the
empirically determined mean maximal weights of 7.8 g
and 11.1g (¢gure 1). These calculations suggest that evolu
tionary changes in these three factors almost completely
account for the evolutionary increase in body size
observed." .
If you're going to cut and paste, pay some attention to the formatting.
But again, this quote isn't relevant to your assertion. It merely shows
what developmental processes are the proximate reason for change. It
doesn't say anything about the hereditary basis of those changes, which
I would expect to be genetic.

We all agree that much of evolution is about development. The question
is the source of those developmental changes, and the manner in which
they are inherited. You have never presented any evidence relevant to
that question. And this is your central problem.

The source of these developmental changes in growth rate , critical
body size and PTTH delay time are all determined in the insect's brain
and epigenetically (computation and processing in the insects brain
is a nongenetic phenomenton, right?)

Some of them, at least. So? You haven't dealt with the essential problem in your argument. Epigenetic developmental phenomena are not in contradiction to genetic differences being responsible for inheritance of changes in those phenomena.

[snip more repetitive and regurgitated examples of irrelevance]
The epigenetic mechanism of inheritance
At last!
The fact that metazoan structure is maintained for considerable
periods of time (during the adult life time), despite the unavoidable
erosion of the structure, indicates that a control system at the
organismic level is operational in metazoans. This is an integrated
control system with the central nervous system (diffuse nervous
systems in lower invertebrates) acting as the controller.
The CNS, the controller of the system, via afferents continually
receives and processes a huge input of data on the state of the system
and, on that basis, assesses the structural losses at the molecular
and cellular level throughout the animal body and sends back
"instructions" by activating appropriate signal cascades for
compensating the losses in structure and order.
In most invertebrates and vertebrates,the CNS accomplishes these
functions via two basic branches:
1. The neuroendocrine branch, the neuroendocrine system, consisting of
the nervous system,of the neurally controlled endocrine glands and,
in vertebrates, of the brain-hypothalamic-pituitary-terminal endocrine
glands axes, and
2. The peripheral branch, represented by nerves pervasively
innervating all parts of the animal body.
The fact that the CNS is capable of assessing deviations form the
normal body structure indicates that it has pertinent epigenetic
information. Thus, in the process of biological reproduction the CNS
acts as an epigenetic system of inheritance. Indeed, there is
overwhelming evidence (an adequate part of that evidence was presented
in three earlier posts of this series) that the central nervous system
controls and regulates reproductive cycles, reproductive behaviors,
the formation of gametes, and the early embryonic development up to
the phylotypic stage. I have provided adequate evidence that this
process of providing epigenetic information to gametes is under neural
control.
The individual development takes place in two main phases:
1.The early embryonic development controlled by parental CNS(s) via
cytoplasmic factors, centrioles and microtubular structures), and
2.The post-phylotypic development controlled by the embryonic CNS
The early individual development from the zygote (egg cell in
parthenogenetic organisms) to the phylotypic stage is under control of
the epigenetic information provided to the egg cells in the form of
cytoplasmic factors, centrioles and microtubular structures.
At the end of the phylotypic stage, the parental epigenetic
information in the embryo is exhausted, but no informational crisis
develops because at this early moment an operational nervous system is
in place.
von Neumann dreamed of a machine (replicator) that would be able to
produce copies of itself if provided with necessary parts. von
Neumann's machine then would install and switch on in the daughter
machine a program, which would enter self-replicating cycles of
producing new von Neumann's machines.
Due to the huge amount of epigenetic information necessary for
erecting metazoan structures, unlike von Neumann's machines,
eumetazoans cannot transmit with gametes the whole program of the
development of the future organism. What they transmit with gamete(s),
instead is not the program but epigenetic information for constructing
a programmer, the central nervous system at the phylotypic stage.
Experimental evidence shows clearly that the epigenetic information
from gametes is responsible for developing the operational CNS, the
"programmer", at the phylotypic stage. It takes over the post-
phylotypic development up to the adulthood in metazoans.
We know that the nervous system, by processing stimuli and other data
on internal and external environment, produces new information by
starting appropriate signal cascades for adapting the organism and for
maintaining the normal state of its thermodynamically unstable
structure, but we still don't know the mechanism of generation of the
new information in the CNS because we still don't know the ways it
computates. We know "what" the CNS does but we don't know "how". In
this respect the situation is now similar to that of genes in the
second decade of the 20 century when, Wilhelm Johanssen, one of the
founders of the classical genetics, said we know what genes do but we
don't know what they are.
Vast experimental evidence shows that the CNS becomes the source of
information for local and global inductions for formation of organs,
tissues and other structures during the whole individual (prenatal and
pos-natal) development until adulthood (see my post Epigenetic Control
of Post-Phylotypic Development , Feb. 12).
So far, nothing about inheritance.
Probably you missed the lines you quoted from my post:
eumetazoans cannot transmit with gametes the whole program of the
development of the future organism. What they transmit with gamete(s),
instead is not the program but epigenetic information for constructing
a programmer, the central nervous system at the phylotypic stage.
Experimental evidence shows clearly that the epigenetic information
from gametes is responsible for developing the operational CNS, the
"programmer", at the phylotypic stage. It takes over the post-
phylotypic development up to the adulthood in metazoans. We know that the nervous system, by processing stimuli and other data
on internal and external environment, produces new information by
starting appropriate signal cascades...
Now, if I say that the metazoan organism transmits to gametes
epigenetic information for constructing the central nervous system,
which takes over the post-phylotypic development and the adult CNS
regulates gametogenesis in repeating cycles is that not inheritance to
you? What then is your definition of inheritance?
It's a ridiculously inadequate mechanism, and your claim wasn't clear.

What do you find ridiculous in that mechanism? You have to argue your
statements.

It's ridiculous because you haven't given any reason to suppose that there could possibly be more information in your transmission mechanism than in the genome.

How are epigenetic changes inherited
The bone of contention in discussions related with this series of
posts on epigenetic information and inheritance is whether there are
nongenetic mechanism by which epigenetic changes can be transmitted to
the offspring. Mr. Harshman has argued that neurally determined
epigenetic factors cannot be inherited because the central nervous
system is not inherited.
Is he right?
As I have pointed out in an earlier post (Epigenetic control of early
development, Feb. 11) the process of neurulation starts very early at
the blastula stage (according to Muller, 1996,), even earlier in the
uncleaved egg, and is the function of epigenetic information
(parentally provided cytoplasmic factors). Formation of the
operational central nervous system is accomplished at the phylotypic
stage, i.e. during the early development that is controlled and
regulated by the parentally provided epigenetic information rather
than by zygotic genome (expression of zygotic genes is regulated by
the parentally provided epigenetic information).
So far, nothing about inheritance. Apparently it's all the nervous
system pulling itself up by its bootstraps.
Read again the paragraph I brought to your attention.
Now, I believe, you understand that the central nervous system is
epigenetically inherites and as Tierney says, it is "a largely
epigenetic
phenomenon."
Who is Tierney? Why can't you give complete citations?

I wish you also held yourself to such lofty citation standards. Here
it is: (Tierney, A.J. 1996. Behavioural Processes 35: 173-182).

There. Was that so difficult?

The full citation is also in my book Epigenetic Principles of
Evolution and in my website.

Now that you haev the citation, can I hope you are going to change
your mind and agree that the CNS is inherited and is epigenetically
inherited? Or it is just to verify my source?

No. In fact Tierney says *nothing* about the epigenetic inheritance of the CNS. It has nothing to do with your thesis. The very paragraph you quoted here actually contradicts one of your claims, in that it says that changes in peripheral organs can induce changes in CNS development. That's the opposite direction of causation from your claims.

"The development of the nervous system is a largely epigenetic
phenomenon." (Tierney, A.J. 1996. Behavioural Processes 35: 173-182
In short, the development of the central nervous ss stem is
epigenetically determined by the epigenetic information deposited in
gametes whereas the deposition of epigenetic information in gametes is
epigenetically determined by the central nervous system. Here on TO,
Perplexed in Peoria expressed this idea (reduced to its essentials) on
the "physiology" of the epigenetic inheritance as follows:
"maternal transcripts and the cytoskeleton of the egg determine the
CNS which in turn determines the maternal transcripts and cytoskeleton
of the next generation's egg."
Ah, the theory begins to emerge. It seems to be, mirabile dictu, exactly
what Perplexed in Peoria predicted: the maternal nervous system
determines some primary transcripts that are deposited in the egg, and
the primary transcripts determine the nervous system, which then
determines everything else. And his objection applies here: you complain
that the genome can't contain enough information to determine
development, yet there is much less information in those deposited
transcripts than in the genome. This is an informational bottleneck
through which your theory can't fit. The differences among species can't
possibly be determined in the way you imagine.
This objection I have seen only in your post when you wrote that there
are just a few maternal factors. This is incorrect: only in the tiny
sperm cell cytoplasm are deposited more than 2500 paternal mRNAs
(Ostermeir et al. 2002. Lancet 360: 772-777), not counting other
cytoplasmic factors, such as secreted proteins, hormones,
neurotransmitters, etc), which are responsible for " a surprising
degree of paternal control" (Wagner et al. 2004. Developmental Cell 6:
781-790). How many cytoplasmic factors may be deposited in the
comparatively huge egg cytoplasm? How many maternal factors can get
access transplacental to embryos?
You seem to be confused about this. Wagner et al. are not talking about
paternal cytoplasmic factors, but about paternal effect genes, i.e.
those expressed in the zygote. I can't see the Lancet article, which has
no abstract.

John, you should know that paternal effect genes are genes that are
expressed in the paternal genome and deposited in the form of paternal
cytoplasmic factors (mainly mRNAs) in the sperm cell. Wagner et al
talk about the "surprising degree of paternal control" that these
thousands of paternal cytoplasmic factors exert on early development.

Not true. Paternal effect genes are generally expressed in the zygote, and are imprinted as paternal genes. Wagner et al. say nothing about paternal transcripts in sperm controlling development of the zygote.

Let me avoid the confusion can cause your statement on the
insufficiency of genetic information for individual development in
metazoans.
I have explained you (and I have calculated for you) here in TO that
there is an amount of quadrillions of bits of information necessary
for erecting a human body, while the amount of the information in
human genome (the whole human DNA, including repetitive sequences and
the "junk DNA) is only about 4 billion bits. This quantitative
obstacle and the qualitative problem that the only thing the genetic
information can do is determine the sequence nucleotides in RNAs and
of amino acids in peptide chains make it impossible to account for the
development of the human body.
The epigenetic information in the form of cytoplasmic factors
deposited in strictly determined patterns is experimentally proven
that directs the the whole early development, including formation of
the first system, the initially simple but operational central
nervous system at the phylotypic stage.
Again, how can cytoplasmic factors that represent a small portion of the
genome contain so much more information than the entire genome?

Evidence shows that the number of cytoplasmic factors (not only, RNAs
but also proteins, hormones, neurotransmitters, neuromodulators, etc.)
in the egg and sperm cells (in nonplacentals) should be smaller than
the number of genes in the genome but the combined number of paternal
and maternal factors in the zygote is certainly larger.

That's nonsense. The zygote has all the genes present in both parents. It will lack some allelic variation, but none of that is relevant for any developmental result that's fixed within a species. Genes expressed in the parents must be a subset of the genome, and thus can't contain more information than the genome.

And it is
experimentally proven that this epigenetic information controls the
early development in metazoans, including formation of the
rudimental but operational central nervous system at the phylotypic
stage.

It certainly has some effect, in some species. But none of this explains the inherited differences among species.

.

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