Re: [asa] The Myth of the Rejected ID Paper (science stoppers and OOL)

From: Rich Blinne <rich.blinne@gmail.com>
Date: Fri Jul 04 2008 - 13:49:24 EDT

On Jul 4, 2008, at 10:47 AM, Murray Hogg wrote:

> And the question would have to be: just how many peer reviewed
> papers are there that defend an identification of irreducible
> complexity in respects of specific biological systems/features?
>
> I can't answer that question, but I suspect the answer is "not
> many". And if that suspicion is right then it perhaps doesn't bode
> well for ID theory as a successful explanatory hypothesis.

Your suspicions are spot on. My Google Scholar searches was for peer-
reviewed articles by the elites of ID on any biological topic
whatsoever. No paper by Dembski see how my explanatory filter applies
to this biological feature. Nor does Behe do the heavy lifting to
prove his point that mutations are statistically independent as he
claims in his more recent non-peer-reviewed book (so that he can
conveniently square the statistics). On the other hand Rich Lenski
created a novel experiment to show otherwise. (www.pnas.org/cgi/doi/10.1073/pnas.0803151105)

> The role of historical contingency in evolution has been much
> debated, but rarely tested. Twelve initially identical populations
> of Escherichia coli were founded in 1988 to investigate this issue.
> They have since evolved in a glucose-limited medium that also
> contains citrate, which E. coli cannot use as a carbon source under
> oxic conditions. No population evolved the capacity to exploit
> citrate for >30,000 generations, although each population tested
> billions of mutations. A citrate-using (Cit+) variant finally
> evolved in one population by 31,500 generations, causing an increase
> in population size and diversity. The long-delayed and unique
> evolution of this function might indicate the involvement of some
> extremely rare mutation. Alternately, it may involve an ordinary
> mutation, but one whose physical occurrence or phenotypic expression
> is contingent on prior mutations in that population. We tested these
> hypotheses in experiments that “replayed” evolution from
> different points in that population's history. We observed no Cit+
> mutants among 8.4 × 1012 ancestral cells, nor among 9 × 1012 cells
> from 60 clones sampled in the first 15,000 generations. However, we
> observed a significantly greater tendency for later clones to evolve
> Cit+, indicating that some potentiating mutation arose by 20,000
> generations. This potentiating change increased the mutation rate to
> Cit+ but did not cause generalized hypermutability. Thus, the
> evolution of this phenotype was contingent on the particular history
> of that population. More generally, we suggest that historical
> contingency is especially important when it facilitates the
> evolution of key innovations that are not easily evolved by gradual,
> cumulative selection.

In short, Lenski tested what Behe implicitly proposed without testing
(that mutations are not contingent on previously selected mutations)
in the Edge of Evolution. If the novel ability of E Coli to metabolize
citrate did not happen for 20 years of the ongoing experiment, then we
are not merely selecting from a pre-existing designed small sample of
E Coli that could do it. Lenski also proved contingency so Behe's
bogus assumption that point mutation rates are statistically
independent is wrong and cannot be squared. Note also that the same
long term evolution experiment (LTEE) have produced the following
results:

> Previous analyses of this experiment have shown numerous examples of
> parallel phenotypic and genetic evolution. All twelve populations
> under went rapid improvement in fitness that decelerated over time
> (2, 3, 22, 23). All evolved higher maximum growth rates on glucose,
> shorter lag phases upon transfer into fresh medium, reduced peak
> population densities, and larger average cell sizes relative to
> their ancestor (22–26). Ten populations evolved increased DNA
> supercoiling (27), and those gene-expression profiles (4, 28, 29).
> At least three genes have substitutions in all 12 populations (30,
> 31), and several others have substitutions in many populations (27–
> 30), even though most loci harbor no substitutions in any of them
> (32). At the same time, there has also been some divergence between
> populations. Four have evolved defects in DNA repair, causing
> mutator phenotypes (3, 33). There is subtle, but significant,
> between-population variation in mean fitness in the glucose-limited
> medium in which they evolved (2, 23). In media containing other
> carbon sources, such as maltose or lactose, the variation in
> performance is much greater (34). And while the same genes of ten
> harbor substitutions, the precise location and details of the
> mutations almost always differ bet ween the populations (27–31).
>
> 2. Lenski RE, Rose MR, Simpson SC, Tadler SC (1991) Long-term
> experimental evolution in Escherichia coli. I. Adaptation and
> divergence during 2,000 generations. Am Nat 138:1315–1341.
>
> 3. Cooper VS, Lenski RE (2000) The population genetics of ecological
> specialization in evolving E. coli populations. Nature 407:736 –739.
>
> 4. Cooper TF, Remold SK, Lenski RE, Schneider D (2008) Expression
> profiles reveal parallel evolution of epistatic interactions
> involving the CRP regulon in Escherichia coli. PLoS Genet 4:e35.
>
> 22. Lenski RE (2004) Phenotypic and genomic evolution during a
> 20,000-generation experiment with the bacterium Escherichia coli.
> Plant Breed Rev 24:225–265.
>
> 23. Lenski RE, Travisano M (1994) Dynamics of adaptation and
> diversification: A 10,000-generation experiment with bacterial
> populations. Proc Natl Acad Sci USA 91:6808 – 6814.
>
> 24. Vasi F, Travisano M, Lenski RE (1994) Long-term experimental
> evolution in Escherichia coli. II. Changes in life-history traits
> during adaptation to a seasonal environment. Am Nat 144:432– 456.
>
> 25. Lenski RE, Mongold JA (2000) in Scaling in Biology, eds Brown J,
> West G (Oxford Univ Press, Oxford, UK), pp 221–235.
>
> 26. Novak M, Pfeiffer T, Lenski RE, Sauer U, Bonhoeffer S (2006)
> Experimental tests for an evolutionary trade-off between growth rate
> and yield in E. coli. Am Nat 168:242–251.
>
> 27. Crozat E, Philippe N, Lenski RE, Geiselmann J, Schneider D
> (2005) Long-term experimental evolution in Escherichia coli. XII.
> DNA topology as a key target of selection. Genetics 169:523–532.
>
> 28. Cooper TF, Rozen DE, Lenski RE (2003) Parallel changes in gene
> expression after 20,000 generations of evolution in Escherichia
> coli. Proc Natl Acad Sci USA 100:1072–1077.
>
> 29. Pelosi L, et al. (2006) Parallel changes in global protein
> profiles during long-term experimental evolution in Escherichia
> coli. Genetics 173:1851–1869.
>
> 30. Woods R, Schneider D, Winkworth CL, Riley MA, Lenski RE (2006)
> Tests of parallel molecular evolution in a long-term experiment with
> Escherichia coli. Proc Natl Acad Sci USA 103:9107–9122.
>
> 31. Cooper VS, Schneider S, Blot M, Lenski RE (2001) Mechanisms
> causing rapid and parallel losses of ribose catabolism in evolving
> populations of E. coli B. J Bacteriol 183:2834 – 2841.
>
> 32. Lenski RE, Winkworth CL, Riley MA (2003) Rates of DNA sequence
> evolution in experimental populations of Escherichia coli during
> 20,000 generations. J Mol Evol
> 56:498 –508.
>
> 33. Sniegowski PD, Gerrish PJ, Lenski RE (1997) Evolution of high
> mutation rates in experimental populations of Escherichia coli.
> Nature 387:703–705.
>
> 34. Travisano M, Vasi F, Lenski RE (1995) Long-term experimental
> evolution in Escherichia coli. III. Variation among replicate
> populations in correlated responses to novel environments. Evolution
> 49:189 –200.
>

As we can see, It's not really a science stopper in the absolute sense
because Lenski and others have continued to practice science while the
small group of ID proponents have not. Thus, the net effect on science
itself is actually quite small while the effect on the community of
faith is incalculable.

Rich Blinne
Member ASA

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Received on Fri Jul 4 13:49:54 2008

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