Dust-up

It’s been awhile since I’ve done an ID post.  Thomas Cudworth on UD goads me thusly:

From June 17 to June 21, 2011, at the University of Oklahoma (Norman) campus, the conference “Evolution 2011” was in session.  It was co-sponsored by three scientific societies – The Society for the Study of Evolution, The Society of Systematic Biologists, and the American Society of Naturalists.  It was billed by its promoters as “the premier annual international conference of evolutionary biologists on the planet.”

…

It is interesting to make a mental list of the Darwin-defenders who have been most active in the culture wars, whether by publishing popular books defending Darwin, by appearing as witnesses against school boards in court cases, by working for the NCSE, by running pro-Darwinian blog sites, or by attacking Darwin critics throughout cyberspace, and to see which of them either read papers or at least contributed to the research and writing of papers for this premier conference.

…

Among those who have not attacked religious belief, but have violently bashed ID and/or passionately upheld neo-Darwinian theory, Paul Gross (co-author of Creationism’s Trojan Horse) and plant scientist Arthur Hunt (who has debated ID people live and on the internet) were not listed as contributors to any of the papers.

…

The theme of my column is qualifications. The question is: are most of the Darwinian preachers in the culture-wars competent to discuss the latest developments in evolutionary biology? If they are not competent, shouldn’t the public know this?

What I’m trying to do here is to give everyone a chance to say whether these people are or are not qualified. And I invite any of the named people — Falk, Venema, Moran, Miller, etc. — to write in here, listing their publications and conference papers in the field of evolutionary biology, and explaining why we should prefer their account of evolution to those of Darwin-critical specialists in evolutionary theory such as Lynn Margulis, Stuart Newman, Richard Sternberg, etc.

Behe and the limits of evolution – revised

[Introductory remark – it was pointed out by a commenter on PT that my use of pollen grains in the original essay was confusing since it implied that the male-sterile phenotype is inherited paternally.  I was trying to squeeze as many genomes as possible into my scenario, to give Behe as much benefit as possible, and I used the numbers of pollen grains rather than kernels to that end.  However, after much reflection, I’ve decided to update the essay and remove the reference to pollen grains when “calculating” things.  I apologize for any confusion my previous discussion may have caused.]

Intelligent Design proponent Michael Behe has recently taken Ken Miller to task for the latter’s rough handling of another ID proponent’s handling of some concepts in evolution.  I don’t intend to add to the back and forth between the two (or three?) of them here.  Rather, I thought I would use one of Behe’s closing remarks as an excuse to repost a (slightly-modified) Panda’s Thumb essay that pertains to one of Behe’s newer calling cards – the so-called “Edge of Evolution”.

Well that was interesting

It’s a closely-guarded secret that can now be revealed – on Friday, May 14, Steve Matheson and I served as the critics for an event at Biola University the focus of which Stephen Meyer and his book “Signature in the Cell”.  (Well, actually, this was the lead-in to some big hoopla about the release of a new Illustra DVD entitled “Darwin’s Dilemma”.  But that will have to be the subject of someone else’s writing, since I didn’t go to the screening, nor did I bother to scarf up a DVD.)

It was probably against my better judgment to do this, but I folded this event in with some other, more professorial activities and managed to have a productive and agreeable visit to Biola.

But this blog entry is about the Signature in the Cell event.  The format for this was a bit different from your usual debate – thus, after the glitzy Meyer presentation, a panel of hand-selected critics (chosen by the event organizers) would be given opportunities to grill Meyer.  In other words, there would be no tit-for-tat here, but rather a one-way exchange of Q&A.  This is roughly what transpired, but in a shorter period of time than I expected.

What follows is a recap (from memory – I didn’t bother trying to scribble down notes while everyone was talking) of the proceedings.  This is intended as much as anything to convey my own impressions, and should not be mistaken for advice or instructions on how to approach things like this.

Signature in the Cell?

There is much abuzz in the ID-o-sphere regarding Stephen Meyer’s new book, “Signature in the Cell: DNA and the Evidence for Intelligent Design”.  The book is a lengthy recapitulation of the main themes that ID proponents have been talking about for the past 15 years or so; indeed, there will be precious little that is new for seasoned veterans of the internet discussions and staged debates that have occurred over the years.

Long though the book is, it is built around one central theme – the idea that the genetic code harbors evidence for design.  Indeed, the genetic code – the triplet-amino acid correspondence that is seen in life – is the “Signature in the Cell”.  Meyer contends that the genetic code cannot have originated without the intervention of intelligence, that physics and chemistry cannot on their own accords account for the origin of the code.

It is this context that a recent paper by Yarus et al. (Yarus M, Widmann JJ, Knight R, 2009, RNA–Amino Acid Binding: A Stereochemical Era for the Genetic Code, J Mol Evol  69:406–429) merits discussion.  This paper sums up several avenues of investigation into the mode of RNA-amino acid interaction, and places the body of work into an interesting light with respect to the origin of the genetic code.  The bottom line, in terms that relate to Meyer’s book, is that chemistry and physics (to use Meyer’s phraseology) can account for the origin of the genetic code.  In other words, the very heart of Meyer’s thesis (and his book) is wrong.

On the utility of evolution in experimental biology and medicine

A recurring theme amongst ID antievolutionists holds that evolution really doesn’t contribute useful directions or concepts in the realm of biology or medicine. Philip Skell regurgitates the theme in a recent commentary in Forbes magazine:

“Examining the major advances in biological knowledge, one fails to find any real connection between biological history and the experimental designs that have produced today’s cornucopia of knowledge of how the great variety of living organisms perform their functions. It is our knowledge of how these organisms actually operate, not speculations about how they may have arisen millions of years ago, that is essential to doctors, veterinarians, farmers and other practitioners of biological science.”

And later:

“The essence of the theory of evolution is the hypothesis that historical diversity is the consequence of natural selection acting on variations. Regardless of the verity it holds for explaining biohistory, it offers no help to the experimenter–who is concerned, for example, with the goal of finding or synthesizing a new antibiotic, or how it can disable a disease-producing organism, what dosages are required and which individuals will not tolerate it. Studying biohistory is, at best, an entertaining distraction from the goals of a working biologist.”

The blogosphere (and probably print media) are replete with summaries and specific cases that show Skell’s assertions to be a crock. This essay summarizes one such example. I have chosen this one because it refutes, specifically, the claim that an understanding of the evolutionary history of an organism “offers no help to the experimenter–who is concerned, for example, with the goal of finding or synthesizing a new antibiotic, or how it can disable a disease-producing organism”. It also ties Skell’s uninformed comments in with another subject that causes ID antievolutionists much consternation – the origins and evolution of organelles.

My response

There’s been a bit of a kerfluffle about a suggestion (challenge) made by a Discovery Institute associate to a professor of biology at the University of Vermont.  The first paragraph:

“Dear Professor Gotelli,

I saw your op-ed in the Burlington Free Press and appreciated your support of free speech at UVM. In light of that, I wonder if you would be open to finding a way to provide a campus forum for a debate about evolutionary science and intelligent design. The Discovery Institute, where I work, has a local sponsor in Burlington who is enthusiastic to find a way to make this happen. But we need a partner on campus. If not the biology department, then perhaps you can suggest an alternative.”

There have been a variety of “responses” to this challenge floating around the blogosphere.  Gotelli himself responded thusly:

Behe and the limits of evolution

Intelligent Design proponent Michael Behe has recently taken Ken Miller to task for the latters rough handling of another ID proponent’s handling of some concepts in evolution.  I don’t intend to add to the back and forth between the two (or three?) of them here.  Rather, I thought I would use one of Behe’s closing remarks as an excuse to repost a (slightly-modified) Panda’s Thumb essay that pertains to one of Behe’s newer calling cards – the so-called “Edge of Evolution”.

In the last paragraph of his response to Miller, Behe says:

“It’s pertinent to remember here the central point of The Edge of Evolution. We now have data in hand that show what Darwinian processes can accomplish, and it ain’t much.”

Actually, as the following essay clearly shows, Darwinian processes can do much more than Behe suggests.  Enjoy.

Axe (2004) and the evolution of enzyme function

[Preface – the subject of protein evolution pops up on a regular basis in ID circles.  Recently, William Dembski mentioned the study alluded to in the title of this essay as an improved argument/piece of evidence for intelligent design.  Specifically, Dembski said:

“(2) The challenge for determining whether a biological structure exhibits CSI is to find one that’s simple enough on which the probability calculation can be convincingly performed but complex enough so that it does indeed exhibit CSI. The example in NFL ch. 5 doesn’t fit the bill. The example from Doug Axe in ch. 7 of THE DESIGN OF LIFE (www.thedesignoflife.net) is much stronger.”

“The example from Doug Axe in ch. 7 of THE DESIGN OF LIFE” would appear to be Axe’s 2004 paper in the Journal of Molecular Biology, the subject of my first ever essay on The Panda’s Thumb.  Since I have been a bit remiss in re-posting older essays here, I thought I would use this excuse to put this here.  It’s “published” without change, so as to maintain some sort of continuity.  As always, enjoy.]

Douglas Axe recently (well, sort of) published an article in the Journal of Molecular Biology entitled “Estimating the Prevalence of Protein Sequences Adopting Functional Enzyme Folds” (Axe, J Mol Biol 341, 1295-1315, 2004). In his discussion of the experimental observations, Dr. Axe mentions some numbers that are likely to generate much discussion amongst Intelligent Design advocates and critics. For example, Stephen Meyer (2004) cites Axe at a key point in the argument in his recent article advocating Intelligent Design, “The Origin of Biological Information and the Higher Taxonomic Categories,” much discussed in previous Panda’s Thumb threads (here).

“Axe (2004) has performed site directed mutagenesis experiments on a 150-residue protein-folding domain within a B-lactamase enzyme. His experimental method improves upon earlier mutagenesis techniques and corrects for several sources of possible estimation error inherent in them. On the basis of these experiments, Axe has estimated the ratio of (a) proteins of typical size (150 residues) that perform a specified function via any folded structure to (b) the whole set of possible amino acids sequences of that size. Based on his experiments, Axe has estimated his ratio to be 1 to 10^77. Thus, the probability of finding a functional protein among the possible amino acid sequences corresponding to a 150-residue protein is similarly 1 in 10^77.”

More recently, Dembski cited Axe in his Expert Witness Report for the Dover trial (see this).

“Recent research by Douglas Axe (see Appendix 3) provides such evidence in the form of a rigorous experimental assessment of the rarity of function-bearing protein sequences. By addressing this problem at the level of single protein molecules, this work provides an empirical basis for deeming functional proteins and systems of functional proteins to be unequivocally beyond Darwinian explanation.”

Given that this subject is often raised by ID proponents (such as this), and that the Biologic Institute (where Axe works) has made some news accounts, it seems appropriate to review Axe’s work. The purpose of this PT blog entry is to try and lay out the study cited above (Axe DD, J Mol Biol 341, 1295-1315, 2004) in a form that is accessible to most interested parties, and to discuss a larger context into which this work might be placed. Needless to say, the grand pronouncements being made by the ID camp are not warranted.

Is macroevolution impossible to study (Part 2)?

The plant kingdom is many things – the basis of agriculture and civilization, a natural laboratory with a stupefying capability in organic synthesis, a source of untold numbers of pharmaceuticals, antimicrobials, herbals, and other chemical playthings, a fascinating range of biological form and function, and an eminently accessible subject for studies of evolution. Along the lines of the last two bullets, one of the more interesting aspects of plants is the range of growth habits that may be adopted. Among these are two sets of contrasting characteristics – annual or perennial, and herbaceous or woody. Differences in these characteristics are among the bases for classification of plant species. For this reason, but also because accompanying morphological differences can be quite considerable, evolutionary changes that involve transitioning between these states are macroevolutionary. Thus, it stands to reason that studying the means by these characteristics evolve amounts to experimental analysis of macroevolution, and understanding the underlying mechanisms constitutes an explanation of macroevolutionary processes.

It is in this light that a recent report deserves some attention. This report, by Melzer et al., describes studies of the functioning of two regulators of flowering in the herbaceous annual Arabidopsis thaliana. These proteins, called SOC1 and FUL, had been known for some time to be involved in the regulation of flowering. Melzer et al. constructed double mutants deficient in the expression of these two proteins, with the intent of understanding the physiological significance of interactions between these two proteins, associations discovered using the so-called yeast two-hybrid assay. Amazingly, soc1 ful double mutants were dramatically different – they had a more woody growth habit, and they behaved like perennials when it comes to reproduction. The abstract from the paper follows this paragraph. The bottom line that is in keeping with the title of the essay – not only can this particular macroevolutionary process be studied experimentally, it can be understood and the corresponding macroevolutionary process recapitulated in a controlled setting.

The abstract:

Plants have evolved annual and perennial life forms as alternative strategies to adapt reproduction and survival to environmental constraints. In isolated situations, such as islands, woody perennials have evolved repeatedly from annual ancestors1. Although the molecular basis of the rapid evolution of insular woodiness is unknown, the molecular difference between perennials and annuals might be rather small, and a change between these life strategies might not require major genetic innovations2, 3. Developmental regulators can strongly affect evolutionary variation4 and genes involved in meristem transitions are good candidates for a switch in growth habit. We found that the MADS box proteins SUPPRESSOR OF OVEREXPRESSION OF CONSTANS 1 (SOC1) and FRUITFULL (FUL) not only control flowering time, but also affect determinacy of all meristems. In addition, downregulation of both proteins established phenotypes common to the lifestyle of perennial plants, suggesting their involvement in the prevention of secondary growth and longevity in annual life forms.

The citation:

Melzer S, Lens F, Gennen J, Vanneste S, Rohde A, Beeckman T. 2008. Flowering-time genes modulate meristem determinacy and growth form in Arabidopsis thaliana. Nature Genetics, published online: 9 November 2008 | doi:10.1038/ng.253

Is macroevolution impossible to study?

Once again, the Discovery Institute is playing word games with educational systems, trying to give legal protection to religion-based incompetence.  I refer, of course, to the ongoing debate about standards in Texas, and the insidious influence that the DI is wielding.

As Wesley Elsberry notes in his summary of the alleged weaknesses of evolutionary theory, an oft-repeated mantra rears its head yet again.  This ID tenet holds that macroevolution is either not possible, or cannot be observed, or cannot be studied (or any combination of the these).  Apparently, Board of Education member Ken Mercer is of the opinion that macroevolution has not been observed.