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Message from discussion Dembski poses 10+1 questions for PZ Myers
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hersheyh  
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 More options Jun 1 2011, 10:58 am
Newsgroups: talk.origins
From: hersheyh <hershe...@yahoo.com>
Date: Wed, 1 Jun 2011 07:58:22 -0700 (PDT)
Local: Wed, Jun 1 2011 10:58 am
Subject: Re: Dembski poses 10+1 questions for PZ Myers
On May 31, 4:22 pm, "Steven L." <sdlit...@earthlinkNOSPAM.net> wrote:

> PZ Myers is going to Glasgow to lecture on evolution.

> Dembski is asking his fans there to attend Myers' lecture and pose the
> following questions to Myers:

> 10+1 Questions for Professor Myers:

Here is how I, with only a little study, would respond:

> 1) In light of the Darwinian evolutionary paradigm, can you account for

In light of Intelligent design, can you explain the reasoning behind

> the observation that the eggs [sic; "embryos"?] of the five classes of
> vertebrate (i.e. fish, amphibians, reptiles, birds and mammals) begin
> markedly different from each other? While the cleavage patterns in four
> of the five classes show some general similarities, the pattern in
> mammals is very different.

Size and the amount of yolk has a great deal to do with the
differences, which are not as great as you claim. Evolution of mammals
from terrestrial organisms that had already evolved such terrestrial
specializations as the amniotic sac also has an important role.

> Furthermore, in the gastrulation stage, a
> fish is very different from an amphibian,while both are starkly
> different from reptiles, birds and mammals, which are somewhat similar
> to each other.

"Very different" is in the eye of the beholder.  All vertebrates form
guts asshole first through invagination (the blastopore in amphibians,
the primitive groove in birds, reptiles, and mammals).  Fish, as
exemplified by the zebrafish (PZ has some familiarity with this
organism ;-) produces a dorsal thickening (the embryonic shield) that
is the functional equivalent of the dorsal blastopore lip of
amphibians.   "If one conceptually opens a Xenopus blastula at the
vegetal pole and stretches the opening into a marginal ring, the
resulting fate map closely resembles that of the zebrafish embryo at
the stage when half of the yolk has been covered by the blastoderm."
http://www.ncbi.nlm.nih.gov/books/NBK10100/
IOW, most of the *differences* are a consequence of egg and yolk size
and the shape of the invagination site rather than any fundamental
difference. Apparently IDiots cannot understand topological homology.

> Doesn’t Darwinism predict a pattern wherein the earliest
> stages are the most similar and the later stages are the most different?

> 2) Kalinka et al. (2010) have documented that the developmental
> hourglass model (which describes the observation that embryogenesis
> within a phylum diverges most extensively during early and late
> development, while converging in the middle) holds true even with
> respect to patterns of gene expression, which has a central role in
> elaboration of different animal forms.  Given that mutations affecting
> the earliest stages of development are the least likely to be
> evolutionarily tolerated,

Can you provide the empirical or theoretical reasoning behind the
above assumption?  Does ID provide an alternative testable explanation
for whatever you think you mean for whatever examples you mean?  Or
does it, like the God of the Gaps it is, simply say that whatever
happens is due to the dyslexic doG?

> would you please explain how you would account
> for this observation in terms of evolutionary rationale?

> 3) Could you please explain the sheer lack of congruence between
> anatomical homology and developmental pathways/precursors? Since such
> congruence is a prediction of neo-Darwinism,why isn’t it observed?

Can you give some examples of what you mean?

> Moreover, not only are there different embryological (i.e.
> non-homologous) processes and different genetic mechanisms to apparently
> homologous organs. But there is also the conundrum of homologous genetic
> mechanisms for analogous (i.e. non-homologous) organs. And then there is
> also the problem of homologous structures arising from different
> embryological sources, utterly undermining the evolutionary explanation.
> Isn’t the most straightforward reading of these facts that the adult
> organs have not been derived from a common ancestor? Why is it that you
> are happy to use those instances where embryological development and
> adult similarities are consistent as evidence of common descent, but set
> aside those instances where they are not consistent?

That is a claim without examples as stated.  Can you provide specific
examples of what you mean?

> 4) Could you please explain the near-total absence of evidence for
> evolutionarily relevant (i.e. stably heritable) large-scale variations
> in animal form, as required by common descent? “Near-total”, that is,
> because losses of structure are often possible. But common descent
> requires the generation of anatomical novelty. Why is it the case that
> all observed developmental mutations that might lead to macroevolution
> (besides the loss of an unused structure) are harmful or fatal?

Can't creationists wrapped in the cheap tuxedo of ID come up with
anything but the old, tired, "evolution must work by magically poofing
some large change into existence or it is impossible"?  Especially
when *their* explanation is that "some dyslexic doG magically poofed
some large change into existence."  The fact is that all major changes
observed in modern vertebrate structure (like wings or hands) are
modifications of pre-existing vertebrate structures.  So, again, what
*specific* examples are they talking about?

> 5) Would you please explain why the purported embryological evidence for
> evolution is not subject to careful cherry picking of data, given that
> instances can be identified in which, for example, tissues arise during
> development in the opposite order from which they are presumed to have
> evolved (e.g. the formation of teeth after the tongue whereas it is
> thought that the teeth evolved first; and various vertebrate organs such
> as liver and lung develop embryologically in quite different ways from
> how it is thought they evolved)?

Why do you think that evolution requires that the timing of
development of a tissue must be the same as the timing of its
evolution?   Oh, I see.  IDiots seem to be stuck in the idea that
modern evolutionists all believe that "ontogeny recapitulates
phylogeny" is a universal law.  I hate to Haeckel you, but "It ain't
true."

> 6) Would you please explain instances of species which possess similar
> adult forms but different immature forms, which could conform with
> recapitulation only if the species evolved convergently?

Perhaps the best example is direct development as opposed to pluteus
development in sea urchins.  Ans: Egg size has a lot to do with it.
What other examples do you propose?  BTW, Rudy Raff has done a lot of
this work.  Hasn't shaken his understanding that evolution explains
the results.
http://members.fortunecity.com/smashx14/urchin.html

> Related to this
> is the observation that similar phylotypic stages and/or adult
> morphologies may be attained by very different developmental routes.
> Don’t such observations demonstrate that the view of development being
> an exclusively divergent process of increased specialisation is false?

Again, no specificity.  If you expect an actual response, you need to
do better than simply make a broad claim/assertion as if it were
'truth'.  And again you seem to have this idea that modern evolution
and evo-devo is nothing but warmed over Haeckel.

> 7) Would you please elaborate on how a reproductively-capable embryo can
> evolve by virtue of successive but slight modification while retaining
> selectable utility at every stage?

Do you mean, for example, like the neotenous salamanders (which are
reproductively-capable embryos)?  In some cases, the embryo simply
does not produce thyroxin (the hormone that triggers conversion to
adult body form) while its reproductive organs continue to mature.  In
those species (axolotl), one can induce adult body form by injecting
thyroxin.  In other species, there is loss of the thyroxin receptor
protein, so, even though the immature forms can produce thyroxin, they
cannot respond to it.  And in yet other species, the change is
facultative and in wet areas, they produce enough thyroxin and in dry
areas they don't.  Notably, the neotenous forms tend to occur in
environments where the land is dry, but there are springs that exist
year around.  Some might attribute that to selective pressure.  But
the genetic "switch" is pretty simple.

And I have already mentioned the pluteus-forming versus direct-
development in sea urchins.  The latter tend to occur in seas where
there has been selection for larger nutrient rich eggs because of
relatively nutrient-poor seas being unable to sustain longer pluteus
development.

> Paul Nelson discussed the concept of
> ontogenetic depth in some detail here and here. He also responded to
> your criticisms of his article, and the somewhat ironic charge of
> quote-mining, here.

> 8 ) On your blog, you have defended the central dogmatist (gene-centric)
> view that an organism’s DNA sequence contains both the necessary and
> sufficient information needed to actualise an embryo’s final morphology.
> If your position is so well supported and the position espoused by
> Jonathan Wells (and others) is so easily refuted, then why do you
> perpetually misrepresent his views? For example, you state “These
> experiments emphatically do not demonstrate that DNA does not matter …
> [Wells'] claim is complete bunk.” Where has Jonathan Wells stated that
> DNA “does not matter”? Moreover, contrary to your assertions, the
> phenomenon of genomic equivalence is a substantial challenge to the
> simplistic “DNA-is-the-whole-show” view espoused by the majority of
> neo-Darwinists.

Who is misrepresenting whom here?  DNA is ultimately the whole show,
but epigenetic phenomena (like differential methylations) do exist.

> Cells in the prospective head region of an organism
> contain the same DNA as cells in the prospective tail region. Yet head
> cells must turn on different genes from tail cells, and they “know”
> which genes to turn on because they receive information about their
> spatial location from outside themselves — and thus, obviously, from
> outside their DNA.

Positional information from cell-cell interaction (or its lack, one of
the first such triggers in mammals involves whether a cell is on the
inside or the outside of the blastocyst), interaction with the
environment, or the presence of positional information molecules in
the egg is clearly important in the differentiation process.  Almost
all that information acts through DNA activation or non-activation and
a cascading or spreading or chain of activity.  Did you have a point?
Development and evolution *both* involve the interaction of an
organism's genome with its environment.  Again, what is your point?
Are you claiming that DNA is irrelevant to some important differences?

> So an essential part of the ontogenetic program
> cannot be in the organism’s DNA, a fact that conflicts with the
> DNA-centrism of neo-Darwinism. Some attempts to salvage DNA programs
> (e.g. Rinn et al.) rely on “target sequences” — molecular zipcodes, if
> you will — of amino acids that direct proteins to particular locations
> in the cell. But such “molecular zipcodes” do not create a spatial
> co-ordinate system, they presuppose it.

There is a difference between "interaction" of organismal genome and
environment and the environment acting completely independently of the
genome to produce an organismal feature.  The formation of a human
embryo is dependent on the cell(s) being inside the blastocyst (that
is, positional information).  If there is no such cell inside, no
embryo forms.  But the positional information "triggers" a difference
in the pattern of genetic information expressed.  It doesn't create
that information.

> 9) If, as is often claimed by Darwinists, the pharyngeal pouches and
> ridges are indeed accurately thought of as vestigial gill slits (thus
> demonstrating our shared ancestry with fish), then why is it that the
> ‘gill-slit’ region in humans does not contain even partly developing
> slits or gills, and has no respiratory function?

Again with the warmed over Haeckel.  Ontogeny only very roughly
correlates with phylogeny.  It does not recapitulate it. Been a long
evolutionary time since mammals needed actual gills for respiration.

> In fish, these
> structures are, quite literally, slits that form openings to allow water
> in and out of the internal gills that remove oxygen from the water.

No. In fish, some of these embryonic structures develop *into* slits
that later *become* gills used for respiration.  Except for the ones
that develop *into* jaws and other structures.

> In
> human embryos, however, the pharyngeal pouches do not appear to be ‘old
> structures’ which have been reworked into ‘new structures’ (they do not
> develop into analogous structures such as lungs).

Because lungs are *analogous* structures, not *homologous* ones.  The
structures homologous to lungs are swim bladders (which evolved from
primitive lungs in certain fish). Both are blood rich outgrowths of
the gut in fish that initially got oxygen from air by *swallowing*
it.  Gills are not useful for oxygen extraction in terrestrial
settings (as any fish flopping on the deck could tell you).  BTW,
amphibians also get a substantial amount of oxygen through their thin
skins and their lungs and associated circulatory systems tend to be
simpler than the lungs of reptiles.

> Instead, the
> developmental fate of these locations includes a wide variety of
> structures which become part of the face, bones associated with the ear,
> facial expression muscles, the thymus, thyroid, and parathyroid glands
> (e.g. Manley and Capecchi, 1998).

Yes.  And don't forget jaws. Did you have a point?

> 10) Why do Darwinists continue to use the supposed circuitous route
> taken by the vas deferens from the testes as an argument for common
> descent when, in fact, the route is not circuitous at all? The testes
> develop from a structure called the genital ridge (the same structure
> from which the ovaries develop in females, which is in close proximity
> to where the kidneys develop). The gubernaculum testis serves as a cord
> which connects the testes to the scrotum. As the fetus grows, the
> gubernaculum testis does not, and so the testis is pulled downward,
> eventually through the body wall and into the scrotum. The lengthening
> vas deferens simply follows. And, moreover, before the vas deferens
> joins the urethra, there needs to be a place where the seminal vesicle
> can add its contents.

Rather ballsy of you to include this.  The question is why is the
testes pulled through the body wall, causing a weak spot where the
intestine can bulge through?  Poor design?  How does ID explain this
other than "Because the dyslexic doG wanted it that way."

> http://www.uncommondescent.com/intelligent-design/10-1-questions-for-...

> Note:  I have omitted the "+1" question because it's an ad hominem
> attack not worth responding to.

> -- Steven L.


 
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