Uncommon Descent Serving The Intelligent Design Community

10 + 1 Questions For Professor Myers

Share
Facebook
Twitter
LinkedIn
Flipboard
Print
Email

When Michael Behe visited the UK, back in November, the Humanist Society of Scotland and the British Center for Science Education wrote up a list of “10 + 1 Questions For Professor Behe” which they subsequently distributed to their ranks of faithful followers. I responded, at the time, fairly thoroughly to the arguments made therein here (to which the BCSE retaliated fairly viciously here).

Since PZ Myers has been invited to visit Glasgow next week (one week from today to be specific), to lecture on the embryological evidence for Darwinism, I took it upon myself to draw up this list of “10 + 1 Questions For Professor Myers”. If you happen to be in the area, and are anticipating attending this event next Monday (which will take place in the Crystal Palace, 36 Jamaica Street, from 7pm), feel free to use the following questions as inspiration for the Q&A session which will follow the talk.

10 + 1 Questions For Professor Myers

1) In light of the Darwinian evolutionary paradigm, can you account for the observation that the fertilised egg 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. 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. 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, 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? 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?

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?

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)?

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? 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?

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? 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. 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. 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.

9) It 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), thus constituting evidence for our common ancestry with fish. But the pharyngeal pouches and ridges (the “gill slit” region) in humans does not develop even partly into gills. In fish, these structures are slits that allow water to enter in and out of the gills that remove oxygen from the water. In human embryos, however, the pharyngeal pouches develop into structures such as the thymus, thyroid and parathyroid glands. If this is the case, then whence the mandate for supposing that these systems are vestigial gill slits?

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.

And finally, the extra credit:

11) How many peer-reviewed papers have you published since setting up your blog, Pharyngula? We think the number’s zero, but it would be nice to get confirmation of this.

Comments
I have to ask about your question number 8 - on the slide that PZ Myers is referencing in your quote, Jonathan Wells wrote at the bottom:
The work by Klotz et al. showed that it was the sperm centrosome, rather than sperm DNA, that mattered.
That would, I imagine, be where Jonathan Wells stated that "DNA does not matter", in the context of the paragraph. Perhaps you should pick a better example of Dr. Myers misrepresenting his opponent?Tacroy
May 30, 2011
May
05
May
30
30
2011
08:28 PM
8
08
28
PM
PDT
Jonathan good questions; also of interest, I ran across this about a week back; The mouse is not enough - February 2011 Excerpt: Richard Behringer, who studies mammalian embryogenesis at the MD Anderson Cancer Center in Texas said, “There is no ‘correct’ system. Each species is unique and uses its own tailored mechanisms to achieve development. By only studying one species (eg, the mouse), naive scientists believe that it represents all mammals.” http://www.the-scientist.com/news/display/57986/bornagain77
May 30, 2011
May
05
May
30
30
2011
08:45 AM
8
08
45
AM
PDT
1 2

Leave a Reply