Text 1167, 148 rader
Skriven 2004-12-22 17:16:00 av Perplexed In Peoria (1:278/230)
Ärende: Re: "Genes are followers
================================



"CNCabej" <cncabej@aol.com> wrote in message
news:cqa5pd$o2f$1@darwin.ediacara.org...
> "Perplexed in Peoria" wrote:
>
> >"CNCabej" <cncabej@aol.com> wrote:
>
> >> 4. To show the material structure where the immense information for
> >erecting
> >> metazoan organisms. The gene theory has clearly failed to do that too
> >> (depending on the species, the amount of genetic information in the whole
> >> genome of metazoans, in the best case,  hardly would represent more than
> >one
> >> thousandth of information for building a metazoan organism). The
epigenetic
> >> theory of heredity shows where that structure is and what it consists of.
> >
> >OK.  I'll bite.  Where (in the gametes) is that structure, and what does it
> >consist of?
>
> There is something special in gametes that enables egg cells (alone in
> parthenogenetic organisms and by union with sperm cell in dioecious
organisms)
> to start the individual development, while all the rest of our cell types
could
> never do.
>
> Developmental biology has shown that this is the epigenetic information that
> multicellulars deposit in gametes consists of maternal cytoplasmic factors,
> gene imprinting (and probably other as of yet unknown factors). These
maternal
> factors start cleavage divisions and later, by controlling and regulating
> activation of zygotic genes in a strictly determined spatial and temporal
> order. But it has not shown how this EPIGENETIC information is generated and
is
> placed in the egg cell. No genetic hypothesis has been ever presented how
this
> takes place
>
> The epigenetic theory claims to have shown the molecular mechanism that makes
> this possible. Let's try to show the origin and flow of that epigenetic
> information in one or two experimentally determined examples.
>
> 1. The insect oocytes take vitellogenin from the hemolymph via the
> receptor-mediated endocytosis (vitellogenin proteins bind to their receptors
on
> the oocyte surface in an endocytic complex of clathrin and alpha-adaptin
> vesicles, which in this form are engulfed in the  oocyte).  It has been long
> ago determined that the uptake of vitellogenin is controlled by a "cephalic
> event" (Handler and Postlethwait, 1977), via the ecdysone [(whose synthesis
is
> under strict cerebral regulation of the neuropeptide PTTH (prothoracicotropic
> hormone)]. In the mosquito Aedes aegypti, "the formation of endocytic complex
> is controlled by juvenile hormone, from the corpora allata" (Raikhel ane
Lea),
> which, as it is known, is regulated by brain allatotropins.
> 2. The canary (Serinus canaria) increases the amount of testosterone
deposited
> in each of the successively laid eggs. This is considered to be an adaptive
> maternal investment that compensates for the disadvantaged latter-hatched
> nestlings. Higher amounts of testosterone increase the viability of the
> hatchling but also increase the mass of the hatching muscle (musculus
> complexus, making thus possible an earlier hatching and higher effectiveness
of
> begging for parentally delivered food. Now where is the role of the CNS? The
> concentration of testosterone in the yolk is regulated by the pituitary
> prolactin, which is itself cerebrally regulated according to the following
> signal cascade: chemical signals generated in the bird's brain by processing
> internal and external stimuli in respective neural circuits '
> prolactin-releasing peptide (PrRP) released by neurons of the solitary tract
'
> hypothalamic secretion of prolactin-releasing factor/prolactin-releasing
> inhibiting factor (PRF/PRIF)' pituitary prolactin(in turkeys prolactin
> synthesis is induced by the neurohormone, vasoactive intestinal peptide
(VIP).
>
> I could go on with other examples, but two examples, I believe, suffice to
show
> that a neural mechanism of control of the generation and storage of
epigenetic
> information in the egg cell exists and is operative. The gene theory of
> heredity is clearly unable to account for the origin of that epigenetic
> information and this is the reason why no one has ever attempted to speculate
> how it is may arise.
>
> I anticipate that at this stage it will be argued that this epigenetic
> information, even if comes from the CNS must be of genetic origin. I believe
I
> have clearly proven it before (February-March of this year), here in sbe,
that
> this information is of NONGENETIC, computational, hence epigenetic origin. If
> it is necessary I would be glad to once again deal with the issue.
>
> Thank you for your constructive input.

I am surprised you found my question "constructive".  The only constructive
aspect to my motivation was that I tried to provide sufficient rope.  Now for
some criticism that you will find it a little more difficult to construe as
"constructive".

Mr. Cabej, you have failed to deliver what you promised by a factor of roughly
10^12, surely something of a record for an sbe crackpot.  You said that you
would
show how the gametes contain 10^3 times as much non-genetic information as
genetic.
Your examples provide two bits of information, which is 10^9 times less
information
than the DNA/genetic information.

I am perfectly happy to go with your claim that the presence or absense of
vitellogenin and/or testosterone in an egg cell is not genetic information,
even
though the structure of vitellogenin is directly specified by the genes and the
structure of testosterone is indirectly specified by them.  In this case, what
we are interested in is whether these substances are present, not how they are
built, and you provide some evidence for CNS involvement in this issue.  OK,
this
is non-genetic information.  But if you are going to claim that these are only
two of 10^12 such cytoplasmic factors, then I hope that you see how the fact
that
vitellogenin is a protein might be relevant to whether your claim is credible.

Your implied claim that no genetic hypothesis has been ever presented to
account
for gene imprinting also surprised me.  I am not a specialist in this subject,
but
I thought that there was a hypothesis that imprinting is implemented by a
pattern
of methyl groups added to nucleotides.  Perhaps you define "genetic"
differently
than I do - I would have called this information "genetic" in that it is
preserved
by mitotic processes, even though it is apparently cleared and refreshed by
meiotic
processes.  But even if I concede that it should be classified as non-genetic,
it
is impossible for the quantity of information conveyed by methyl groups to
exceed
the base pair information quantity.
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