Recently in Irreducible Complexity Category

Apparently, Michael Behe just doesn’t know when to pack it in. In reply to Travis’s essay in Science, “On the Origin of The Immune System” (see previous PT posts: 1, 2), Behe has posted a letter he sent to Science. Instead of just sucking it up and admitting that his statements in Darwin’s Black Box that

“As scientists we yearn to understand how this magnificent mechanism came to be, but the complexity of the system dooms all Darwinian explanations to frustration.” (Darwin’s Black Box, p. 139)

and

We can look high or we can look low, in books or in journals, but the result is the same. The scientific literature has no answers to the question of the origin of the immune system. (Darwin’s Black Box, p. 138)

…were wrong, or at the very least became wrong in the time between 1996 and 2005, Behe is still expressing proud, Kierkagaardian-esque defiance. In this (rejected) letter to the editor of Science, Behe reiterates his proud stand that the work of an entire field, the life’s achievements of hundreds of immunologists, complete with surprising experimental support for a surprising hypothesis (the transposon hypothesis), still has “no answers” to the question of how it evolved, and that Darwinian explanations are “doom[ed].”

.. I might add a few brief notes. After Carl Zimmer’s Unicycle-bicycle transitional form, the detailed rebuttal by Keith Ken Miller (Part 1, Part 2 and Part 3), and Nick Matzke revealing that Behe wrote the Pandas’s clotting chapter that Luskin dismisses, there is not much left for me to add*.

I want to highlight two things though. One is a quote that keeps turning up in discussions of Behe’s concept of Irreducible Complexity.

Just as none of the parts of the Foghorn system is used for anything except controlling the fall of the telephone pole, so none of the cascade proteins are used for anything except controlling [he formation of a blood clot. Yet in the absence of any one of the components, blood does not clot, and the system fails. (Behe 1996, pp. 85-86)

Actually, the clotting cascade proteins do have functions other than clotting, indeed Casey’s so-called “Irreducible Core” proteins have other important functions. I go into greater detail in this post about how these functions may have pre-adapted the clotting proteins for their role in clotting. This exposes a major flaw in the concept of irreducible complexity (read the post for the full argument).

Casey also chides Miller for not doing any knock-out experiments on blood clotting systems. This is heavily ironic as no ID proponent, not even Behe, has done any experiments on the blood clotting system. As I point out in my post Behe vs Lampreys+, it’s the evolutionary biologists that have been doing all the heavy lifting in regard to understanding the clotting system. In fact I issued a challenge to the ID proponents, the Amphioxus genome had just been published at http://genome.jgi-psf.org/Brafl1/Brafl1.home.html. Amphioxus is a primitive chordate, more primitive than lampreys, that clot their haemolymph. I challenged the ID proponents to predict which coagulation factors are present in Amphioxus, search the Amphioxus genome database and report on whether the genes found match their predictions.

Since then, silence. I can tell you one thing for sure. The Amphioxus has no gene for fibrinogen, the final step in the modern clotting cascade, yet it still clots its haemolymph. So the very basis of the “Irreducible Core” that Casey goes on about is absent in these animals, and one of Behe’s iconic pathways is exposed as reducible.

Notes:
UPDATE: Yeah, yeah: I can’t spell when writing at 1 am in the morning. But the most embarrassing bit was I got Ken Miller’s name wrong (sorry Ken). Still, the science is right.
* I could have contributed sooner, but I could be playing frisbee on the beach with my kids or surfing the internet. Guess which one I chose.
+This post also has a very nice diagram of the reducibly complex clotting system that Ken Miller discusses (section 4, “An Irreducible Core”). This diagram looks eerily similar to the diagram that Casey uses, as he copied the diagram that I provided for Barbara Forrest and Paul Gross for “Biochemistry by design,” Trends in Biochemical Sciences, Vol. 32(7):301-310 (2007). He’s made a few minor modifications (hint Casey, the correct citation method is “diagram redrawn from” not “information obtained from”), but if he asked nicely, I could have given him the original diagram.

(The following is a slight adaptation of this essay. Readers may post questions and/or comments there as well as here.) As this series of essays has explained, the polyadenylation of messenger RNAs is a vital aspect of gene expression in eukaryotic cells (and a not-so-unimportant facet of RNA metabolism in other contexts). Polyadenylation is mediated by a sizeable complex that includes various RNA-binding proteins, nucleases, and other interesting activities. Genetic studies in yeast indicate that virtually every subunit of the core complex is essential - for viability and for pre-mRNA processing and polyadenylation in vitro and in vivo. (This review is freely available and serves as a good starting point for readers who wish to explore the subject further.) Biochemical and/or immunological depletion studies reveal a similar scenario in mammals, and a less-expansive set of studies suggests that a similar rule of thumb will apply in plants. The bottom line of all of this is that almost all of the subunits of the polyadenylation complex seem to be essential - remove one, and the complex cannot function. In the vernacular of a proponent of intelligent design, the polyadenylation complex would seem to be irreducibly complex.

It is in this context that the recently-completed genome of the parasitic organism Giardia lamblia enters the fray. Last year, the complete sequence of G. lamblia, some 12 million base pairs, was determined and analyzed. The authors of the study published in Science noted a number of interesting things - a preponderance of genes encoding protein kinases, evidence for substantial horizontal gene flow from bacteria and archaebacteria, and a streamlined core gene expression machinery (transcription and RNA processing). This streamlining is especially notable in the case of the polyadenylation machinery. Remarkably, of all the subunits in the yeast complex, genes for only three* can be found in G. lamblia (see the figure that follows this paragraph - adapted from Fig. 1 of Morrison et al.).

The core concept of Dr. Michael Behe’s recent book “The Edge of Evolution” (Behe, 2007) is that protein-protein binding sites are extremely unlikely to have developed by natural means, and therefore were designed by unknown intelligent agents. There is a lot of interest in this concept, as the tag cloud at PT indicates. A recent paper (Grueninger et al., 2008) on human design of binding sites undermines some of his key assumptions, but what is more interesting is an old paper cited in Grueninger that shows researchers have known for some time that evolution of protein-protein binding sites is not as difficult as Behe makes out. Indeed, his very premise was invalid from the beginning.

We learn at the Discovery Institute Blog about a recent lecture tour in Spain by ID creationists

Over an eight day period last January, Physicians and Surgeons for Scientific Integrity (aka DoctorsDoubtingDarwin.com, a rapidly growing, 277-member, physician group from 17 countries) sponsored a lecture tour in Barcelona, Malaga, Madrid, Leon and Vigo. It was titled “Lo Que Darwin No Sabia,” or “What Darwin Didn’t Know.” Tom Woodward, Ph.D. (author of Doubts About Darwin and Darwin Strikes Back) and myself (author of What Darwin Didn’t Know and Billions of Missing Links) lectured on eight occasions to exceptionally large audiences. Santiago Escuain was our translator extraordinaire. Rich Akin, the CEO of PSSI, put in enormous hours into making this trip a huge success.

El Pais reports on the ‘successful’ Spain Tour of ‘Lo que Darwin no sabía’. Of course, the DI does admit later on that the success was limited.

Dear Dr. Behe

Reflecting on your previous post, and the current one, I would like to note that both your mutation rates (10^-4) and effective population size (10⁹-10¹⁰) are too high. By a factor of around a hundred thousand.

The commonest estimates for HIV mutation rates are between 1x10^-5 and 4x10^-5, with 2.5x10^-5 the most common. Well, what’s a half log unit between friends? More serious is your population size estimate. Here I’d like to introduce you to the concept of effective population size.

Dear Dr. Behe

I’m sorry you couldn’t follow Ms Smith’s argument. I found it quite easy, an elegant detective story that built up its case clue by clue. However, even if you couldn’t follow it, the viroporin story was pretty hard to miss. That Vpu evolved over the space of a decade, when viral numbers were low, into a viroporin, a multisubunit structure with a function previously absent from HIV-1, was an obvious key challenge to your assertions.

Dear Dr. Behe

Abbie Smith has recently responded to your reply to her article on the HIV-1 protein Vpu. To refresh your memory, Ms Smith showed that the recently evolved viroporin activity of HIV-1 Vpu directly contradicts your statement that HIV has evolved no new binding sites since it entered humans (see “Edge of Evolution”, page 145 and 146). I see you intend to reply to my open letter at your Amazon blog, rather than engaging in open discussion here, or better yet, doing Ms Smith the courtesy of replying on her own blog. I hope that at least this time you will reply to the key argument Ms Smith made:

HIV-1 M Vpu is a viroporin.

SIV Vpu is not a viroporin, HIV-1 O Vpu is not a viroporin. This is a new activity that evolved in HIV after the split from SIV over a 10 year timeframe and is part of the reason that the HIV-1 M clade is the most common type of HIV in the world.

In the post about my review of Behe’s The Edge of Evolution, many complained that they couldn’t access the full text without a university subscription or paying a huge fee. I have checked Elsevier’s policies on this. Authors are not allowed to post the published PDF to their websites (you have to get that from Elsevier), but they can put up the unformatted, submitted preprint version of their articles, as long as they include the reference and DOI to the published version. So here is the reference: Nicholas J. Matzke (2007). “The edge of creationism.” Trends In Ecology and Evolution, In Press, Corrected Proof, Available online 24 October 2007. ScienceDirect, doi: 10.1016/j.tree.2007.09.004.

…and the full text is below the fold. Note that the unpublished version has a few minor differences from the published version. For example, it has more emphases which were kind of my way of jumping up and down on the smoking ruins of Behe’s core arguments in The Edge of Evolution.

I am pleased to announce that Trends in Ecology and Evolution (TREE) has just put up the article-in-press version of my book review of Michael Behe’s The Edge of Evolution. Here is the reference and link:

Nicholas J. Matzke (2007). “The edge of creationism.” Trends In Ecology and Evolution, In Press, Corrected Proof, Available online 24 October 2007. ScienceDirect, DOI.

The DOI link doesn’t seem to be working just yet, presumably that is temporary. And the other link is one of those nasty superlong ones, so if nothing works, go to the TREE website and click on “Articles in Press” to see it (you will have to have a subscription or university access to get the article; I will provide a partial quote below).

Writing this review was challenging. There are a great many things wrong with Behe’s book, and attempting to hit the most important points effectively, with just 750 words to work with, was quite a challenge. For example, there was no way to fit in anything about HIV, even though some really good points have emerged on that front in the last few months. Thanks to the PT crew for a great many helpful discussions, comments, etc. I also had Cavalier-Smith’s (1997) TREE review of Darwin’s Black Box, literally the article that got me into ID criticism in a serious way, to inspire me (despite some flaws in that review).

I tried to make every word count, so it is hard to pick a summary quote, but here is a bit from the middle:

Laurence Moran at Sandwalk comments on a video excerpt with Bill Dembski, recently touted by the Discovery Institute’s Robert Crowther. What is fascinating that despite more than a decade of Intelligent Design ‘research’ this is the best ID has to offer.

Ironically, Dembski starts of by stating that “what darwinists have done is hidden behind complexities of living systems”. How ironic can this be… While science, as I have shown in several examples, deals in explanations, pathways and hypotheses, Intelligent Design has contributed exactly zero to our scientific understanding of these systems. Worse, while Dembski mentions some complex systems, he also avoids some examples of complex systems science understands quite well how they may have evolved.

My thanks to Robert Crowther for presenting the “best’ response ID has to offer. You be the judge.

On ERV’s blog we find an article titled Irreducible Complexity Reflects Human Ignorance about Phillip Klebba, Professor of Chemistry and Biochemistry at the University of Oklahoma. It was Klebba’s relentless questions during the Q&A of Dembski’s talk at the Trinity Baptist Church Oklahoma University in Norman Oklahoma which forced Dembski to admit to the level of ignorance that is required for ID.

The Baptist Trinity Church had invited Dembski “to penetrate the university campus with the gospel” (source). After all, what better way to introduce the students to the gospel than through the ideas of William Dembski? Dembski presented a talk titled “Why Atheism is no Longer Intellectually Fulfilling: The Challenge of Intelligent Design to Unintelligent Evolution”. During the Q&A, Dembski found out that the students were not impressed by his arguments. While Dembski may have contributed to the successes of Atheism on the University, he also managed to show to the audience present why ID is scientifically vacuous.

Well, my own personal copy of Michael Behe’s new book The Edge of Evolution arrived via amazon.com today, so I suppose it is fair game. I have linked to a few early blog comments (see more from ERV), and Michael Ruse has a short newspaper comment out today. And several other reviews are coming out in the near future in Science, Discover, etc. None of them positive at all, but it’s amazing how much attention someone can get by sacrificing scientific rigour and inserting divine intervention instead.

I don’t have a full review of the book and I won’t for a bit since I am working on other things. But I want to get dibs on one peripheral but particularly shocking and egregious error that Behe makes in The Edge of Evolution. The error is simple but it points to what I have become convinced is the true core of the mishmash known as “intelligent design”: sloppiness and wishful thinking.

Review copies of Michael Behe’s new book The Edge of Evolution are now out – the book is officially coming out on June 5 – and now the reviews are starting. Mark C. Chu-Carroll at Good Math, Bad Math, has beat us all to the punch. I perceived many of these problems while giving The Edge of Evolution my own read-through, but it takes a mathematician to comment on Behe’s abuse of fitness landscapes and probability arguments with the appropriate sense of outrage.

I am sure we will have much more on Behe’s latest starting in June. My first take is that The Edge of Evolution is basically an incompetent attempt to provide a biological foundation for the silly assumptions that were made in Behe and Snoke’s (2004) mathematical modeling paper in Protein Science. (You will recall that it received its most thorough critique here at PT and also in a rebuttal written in Protein Science by Michael Lynch; and a biological rebuttal in this 2006 paper in Science – see also summary by Adami.)

The PNAS Early Edition webpage has just posted a series of papers from the December 2006 National Academy of Sciences Sackler Colloquium, “In the Light of Evolution: Adaptation and Complex Design,” organized by Francisco Ayala and John Avise. The series of papers, on topics ranging from color vision to beetle horns, is now available (I will post the list below the fold). Eugenie C. Scott (aka Genie) was invited to speak at this meeting about evolution education and the history of opposition to it, and the speakers wrote papers to be published in PNAS and a forthcoming NAS volume.

Genie brought me on as a coauthor on the paper she was asked to write. This became:

Although many have read the transcripts of the Kitzmiller v. Dover trial (HTML version | PDF version) and found them interesting, reading the transcripts does not give the full sense of what it was like to be in the Kitzmiller courtroom. In real life, in addition to the witness answering questions, the lawyers and witnesses were constantly referring to exhibits that were digitally projected onto a large screen on the right wall of the courtroom. Usually the exhibits were just documents, but when the science witnesses testified, their powerpoint presentations contain fossils, flagella, and everything else in between. I think it is safe to say that the testimony is much easier to understand when read with the demonstrative exhibits available (the exhibit lists and a few exhibits are available online).

However, it takes a lot of work to convert the slides to web format, add captions, embed them in HTML, etc. But as a first step, I and others at NCSE have done this for Kevin Padian’s testimony (testimony+slides | just slides).

There has been a spate of interest in the blogosphere recently in the matter of protein evolution, and in particular the proposition that new protein function can evolve. Nick Matzke summarized a review (reference 1) on the subject here. Briefly, the various mechanisms discussed in the review include exon shuffling, gene duplication, retroposition, recruitment of mobile element sequences, lateral gene transfer, gene fusion, and de novo origination. Of all of these, the mechanism that received the least attention was the last – the de novo appearance of new protein-coding genes basically “from scratch”. A few examples are mentioned (such as antifreeze proteins, or AFGPs), and long-time followers of ev/cre discussions will recognize the players. However, what I would argue is the most impressive of such examples is not mentioned by Long et al. (1). Below the fold, I will describe an example of de novo appearance of a new protein-coding gene that should open one’s eyes as to the reach of evolutionary processes. To get readers to actually read below the fold, I’ll summarize – what we will learn of is a protein that is not merely a “simple” binding protein, or one with some novel physicochemical properties (like the AFGPs), but rather a gated ion channel. Specifically, a multimeric complex that: 1. permits passage of ions through membranes; 2. and binds a “trigger” that causes the gate to open (from what is otherwise a “closed” state). Recalling that Behe, in Darwin’s Black Box, explicitly calls gated ion channels IC systems, what the following amounts to is an example of the de novo appearance of a multifunctional, IC system.

Over at the Discovery Institute’s Media Complaints Division, Michael Behe seems to be a wee bit concerned by the attention that a recent Nature paper is getting, moaning that, “It seems some scientists have discovered that one way to hype otherwise-lackluster work is to claim that it discredits ID.”

OK. To start with, watching Michael Behe whine about someone else using ID to hype “otherwise-lackluster work” creates a concentration of irony so dense that four mining firms have put in bids for that post. Sorry, but I had to get that one out of my system. Now that I’ve more or less managed to get that minor issue out of the way, let’s look at what, for lack of a better term, we will have to call the “substance” of Behe’s complaints.

Read more (at The Questionable Authority):

On UcD, the following statement by Behe is being discussed. I will show that IC or falsification of IC has nothing to do with Intelligent Design since IC is merely a negative statement about natural selection, and flawed by definition. Nevertheless, this is a good opportunity to expose the fallacies behind ID think and educate people about its flaws and why it has remained scientifically vacuous.

Behe Wrote:

The National Academy of Sciences has objected that intelligent design is not falsifiable, and I think that’s just the opposite of the truth. Intelligent design is very open to falsification. I claim, for example, that the bacterial flagellum could not be produced by natural selection; it needed to be deliberately intelligently designed. Well, all a scientist has to do to prove me wrong is to take a bacterium without a flagellum, or knock out the genes for the flagellum in a bacterium, go into his lab and grow that bug for a long time and see if it produces anything resembling a flagellum. If that happened, intelligent design, as I understand it, would be knocked out of the water. I certainly don’t expect it to happen, but it’s easily falsified by a series of such experiments.

Note that Behe’s claim does not logically follow: Namely that if something cannot be explained by one of the processes of evolution, namely natural selection that we then have to assume that it was intelligently designed. Even though we have no competing explanations as to who, what, how or when. In other words, ‘intelligently designed’ becomes a place holder for our ignorance.

On Nobel Intent, John Timmer discusses amongst others the contrived dualism of many ID relevant claims

He also relied a lot on the “contrived dualism” argument: design was supported by the failure of evolutionary explanations, because no other alternative was possible. This was stated with extraordinary specificity when Behe answered questions, as he more or less claimed that ID was accessible to experimental studies because finding the limits of evolution would reveal design (more on that later).