Re: [asa] ID is not "scinece" because...

On Tue, May 6, 2008 at 4:37 PM, Dehler, Bernie
<bernie.dehler@intel.com> wrote:
Casey Luskin says the Discovery Institute suggested to the Dover Board
that ID not be taught- just the criticism of evolution be taught. I
asked Casey for a textbook, talking about Panda's, and he persuaded me
not to get Panda's, but instead the "Exploring Evolution" book which
only covers evolution criticism along with basic evolution.

The Discovery Institute doesn't suggest ID be taught in schools- from
their web:

http://www.discovery.org/csc/topQuestions.php

(Notice they are not pushing ID at all for schools- since they don't
have a textbook for ID that they are proud of)

They appear to want it both ways. FTE has Bill Dembski as its academic
editor and the domain contact for fteonline.com lists the following e-
mail: dembski@discovery.org. So, what does FTE says is the proper use
of Pandas?

http://www.fteonline.com/pandas-people.html

A supplement to the high school biology textbooks presenting the
scientific rationale for intelligent design as an alternative to
Darwinism.

So, the public face is this but they told the Dover board not to use
it?!?? Why leave the school board in legal jeopardy when DI could
just have gone down the hall and told Bill Dembski to knock it off?
And it's worse than that because my quote I accessed today. So, they
know what happened to the Dover Board but Dembski and FTE are still
pitching the book to high schools when DI says they shouldn't.

Speaking of Dover. Explore Evolution says this:

Finally, you should know something about us, the authors. Two of us
are biology professors doing research on evolution-related topics. Two
of us are philosophers of science who have specialized in studying the
logic of evolutionary arguments. One of us is a science curriculum
writer. All of us happen to have reservations about various aspects of
contemporary evolutionary theory, but we all think that students
should learn more—not less—about this theory than they presently do.
So, while we present criticisms of the theory that many biology books
don't present, we also explain and develop the arguments for
contemporary Darwinian theory in more detail than other standard
textbooks.

Scott Minich in Dover said this:

[495]Q. Please tell us your experience with regard to that quote that
nothing makes sense in biology in light of evolution.

[496]A. In my entire academic training as an undergraduate or graduate
student or as a post-doc at Purdue and Princeton University, I never
once took a formal course in evolution. In fact, when I requested it
as a graduate student, you know, to include it on my graduate student
study plan, it was refused by my committee with a, you know, you don't
have time to do it, it's not necessary.

So that has been my experience as a biologist and a practicing, you
know, experimental biologist, I've never been required to take a
single course in evolution. My exposure formally was in my
undergraduate 100 and 200 level introductory biology classes were we
got basic evolution, you know, Haeckel's embryos, peppered moths,
founder effect. So the basis tenets were there, but in terms of really
looking at this in detail, I haven't.

How in the world can you do "evolution-related research" without
really looking at evolution in detail? Isn't that the canonical
definition of "sloppy research"? What about his research on evolution-
related topics? Again Dover:

Q: And the paper that you published was only minimally peer reviewed,
isn't that true?
A. For any conference proceeding, yeah. You don't go through the same
rigor. I mentioned that yesterday. But it was reviewed by people in
the Wessex Institute, and I don't know who they were.

Let's look at this paper because not only is it one of the few papers
that actually deals with evolution but it also refers to the only
other paper tangentially involving evolution co-written by Minnich.

> Based on these [unpublished] results, we predicted that recent
> atypical virulent strains of E. coli O157:H- (nonmotile) would
> contain a similar genetic lesion. Indeed, this clonal isolate
> carriers a 12-base pair in-frame deletion in flhC [15]. [RDB note:
> unpublished predictions are worthless both in prophesy and in science]

Maybe my note was too harsh. So, did the prediction referenced above
drive how they found the frame deletion? No just standard evolutionary
theory. Here's reference 15 co-written by Minnich. The following is
part of the discussion of the search for the reason for loss of
motility.

> Previously [in 1999], the fliC gene of 493-89, a German SF O157
> strain, was reported to contain two single-site nucleotide
> insertions that produced a frameshift mutation that could,
> presumably, account for the loss of motility (30). [RDB note: in the
> prediction game first to publish wins.]

How was this done in 1999 [from reference 30]?

> To study the molecular evolution of flagellin, the protein subunit
> specifying flagellar (H) antigens, the fliC genes from 15 pathogenic
> strains of Escherichia coli were amplified by PCR and sequenced.
> Comparison of fliC sequences of H6 and H7 strains revealed that
> alleles have a mosaic structure indicating the occurrence of past
> horizontal transfer of DNA segments between strains. The close
> similarity of H7 sequences also indicates the exchange of an entire
> fliC H7 allele between distant clonal lineages. In addition, the
> ratio of silent substitutions to amino acid replacements suggests
> that a short segment in the central region of fliC has been under
> positive selection in the divergence of H6 and H7 alleles.
> Phylogenetic analysis demonstrates that the fliC sequences of
> O157:H7 and O55:H7 serotypes are nearly identical and highly
> divergent from those of E. coli strains expressing H6 and H2
> flagellar antigens. A nonmotile clone of sorbitol-fermenting O157
> has rapidly accumulated multiple mutations in fliC, presumably as a
> result of the silencing of flagellin expression.

What else does Minnich's earlier paper say?

> The fact that the German SF O157 strains carry the H7fliC gene (16)
> and can be manipulated to produce the H7 antigen also confirms their
> close genetic relation to O157:H7 (13, 21) and is in agreement with
> our evolution model that they diverged from O157:H7, in part, by the
> loss of motility (13, 26).

Who is the our here? Is it Minnich and Meyers? What is the evolution
model? Is it irreducible complexity? No on both counts. References 13
and 26 are written by P Feng the main author of the paper. Here's the
abstract of reference 13, entitled Genotypic and phenotypic changes in
the emergence of Escherichia coli O157:H7.

> Escherichia coli O157:H7 is a foodborne pathogen distinguished from
> typical E. coli by the production of Shiga toxins (Stx) and the
> inability to ferment sorbitol (SOR) and to express beta-
> glucuronidase (GUD) activity. An allele-specific probe for the GUD
> gene (uidA) and multilocus enzyme electrophoresis were used to
> elucidate stages in the evolutionary emergence of E. coli O157: H7.
> A point mutation at +92 in uidA was found only in O157:H7 and its
> nonmotile relatives, including a SOR+ O157:H clone implicated in
> outbreaks of hemolytic-uremic syndrome in Germany. The results
> support a model in which O157:H7 evolved sequentially from an O55:H7
> ancestor, first by acquiring the Stx2 gene and then by diverging
> into two branches; one became GUD- SOR- , resulting in the O157:H7
> clone that spread worldwide, and the other lost motility, leading to
> the O157:H clone that is an increasing public health problem in
> Europe.

Here's reference 26.

Genetic and evolutionary analysis of mutations in the gusA gene that
cause the absence of beta-glucuronidase activity in Escherichia coli
O157:H7.

> Escherichia coli serotype O157:H7 do not exhibit beta-glucuronidase
> (GUD) activity but carry the gusA gene (uidA) that encodes for GUD.
> In trans-complementation, the gusA gene cloned from the GUD-positive
> variant strain 493-89 effectively restored GUD activity in O157:H7
> strain 35150. Comparison of gusA sequences from the GUD-negative
> 35150 strain to that of 493-89 revealed several base mutations,
> including a guanosine (G) dinucleotide insertion that caused a
> frameshift in the 35150 gusA gene and introduced a predicted
> premature termination codon. This explains the absence of GUD
> activity in O157:H7. A 35150 gusA construct from which the G-G
> insertion was deleted restored activity in GUD-negative O157:H7
> transformants. The G-G insertion was present in all GUD-negative
> O157:H7 strains but was absent in their GUD-positive variants. The G-
> G insertion that produced the characteristic GUD-negative phenotype
> to O157:H7 strains appeared later than the other gusA mutations in
> the evolutionary emergence of O157:H7.
>

What was the paper's conclusion?

> In conclusion, nonmotility of the German SF O157 strains is due to a
> 12-bp deletion in the flhC gene of the flhDC master regulator
> operon. Specifically, phenylalanine 126 in FlhC appears to be the
> critical amino acid whose deletion resulted in an aberrant protein
> structure that could no longer function as a transcriptional
> activator for motility. The highly conserved nature of the 12-bp
> flhC deletion in the German SF O157 strains may be a useful marker
> for identifying these strains and also supports not only the
> clonality of the German SF O157 strains but also its postulated
> evolutionary divergence from O157:H7. Furthermore, this study has
> identified yet another pathogen that has selectively sustained a
> mutation that down regulates flagellar biosynthesis to, perhaps,
> eliminate competitive interactions between secretory pathways as
> well as the unnecessary expenditure of cellular energy, thereby
> resulting in a more virulent phenotype, a trend being more
> frequently observed among other bacterial pathogens.

I put in bold those "details" that makes sense in biology only in
light of evolution that Minnich apparently missed in a paper he was a
co-author of. Why is understanding evolution important for a
researcher specializing in pathogenic microbes? Because of the
chilling last phrase "a more virulent phenotype, a trend more
frequently observed among other bacterial pathogens". If
microbiologists do not or will not understand evolution people die.
What did I just do? I did what a real peer reviewer would do on a
first pass and do a reference check, seeing whether the references
actually support the conclusions.

What about Robert Seelke? All the papers that Robert Seelke wrote
appear to be in the 80s. Just to verify that there was not any recent
research I did a Google Scholar search which came up with this:

> Your search - author:r-seelke - did not match any articles published
> since 2003.

How about the rest of the community since 2003?

>> Results 1 - 10 of about 478,000 for evolution [definition]. (0.15
>> seconds)

There's your biologists. Maybe they are better educators than
researchers. They say they "develop the arguments for contemporary
Darwinian theory in more detail than other standard textbooks." Yeah,
right. Compare this:
http://www.evolution-textbook.org/content/free/book/toc.html with
this: http://www.exploreevolution.com/table_of_contents.php

Finally, eighty pages is spent on common descent. At least couldn't
they have gotten Michael Behe to write the pro-common descent sections?

Rich Blinne
Member ASA

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Received on Wed May 7 06:05:28 2008