Recently in Irreducible Complexity Category

This has been obvious from the start, but as far as I know it has taken 10 years for the ID guys to finally admit it. Winston Ewert writes at the Discovery Institute blog:

However, Felsenstein and English note that a more realistic model of evolution wouldn’t have a random fitness landscape. Felsenstein, in particular, argues that “the ordinary laws of physics, with their weakness of long-range interactions, lead to fitness surfaces much smoother than white-noise fitness surfaces.” I agree that weak long-range interactions should produce a fitness landscape somewhat smoother than random chance and this fitness landscape would thus be a source of some active information.

GAME OVER, MAN. GAME OVER! The whole point of Dembski et al. invoking “No Free Lunch” theorems was to argue that, if evolutionary searches worked, it meant the fitness function must be designed, because (logical jump herein) the No Free Lunch theorems showed that evolutionary searches worked no better than chance, when averaged over all possible fitness landscapes.

Emergency backup arguments to avoid admitting complete bankruptcy below the fold, just so I’m not accused of leaving out the context.

Once again, desperately dissing Avida

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One of the characteristics of a pseudoscience is repeating discredited arguments as though they were new. And sure enough, once again an Intelligent Design Creationist is flailing around trying to discredit research in digital evolutionary models that shows that structures displaying IDC’s central concept, irreducible complexity, are evolvable via Darwinian processes. I have previously looked at earlier attempts to discredit that research; see here and here for examples.

Now it’s happening again. This month, Winston Ewert, affiliated (according to the paper) with the Discovery Institute’s Biologic Institute (though he doesn’t appear on their published list of personnel), published a review and critique of several computer models of evolution in the DI’s captive journal Bio-Complexity. Ewert was a graduate student of Robert Marks at Baylor, where he was associated with Marks’ and Dembski’s Evolutionary Bioinformatics Lab. He now has a Ph.D. from Baylor, the first in Baylor’s combined electrical engineering and computer science graduate program.

In his critique Ewert looks at five programs: Avida, Tom Schneider’s Ev, Dave Thomas’s Steiner tree GA, Suzanne Sadedin’s geometric model, and Adrian Thompson’s “digital ears”, a program realized in field programmable gate arrays. Here I will analyze Ewert’s critique of Avida; I am less familiar with the other models Ewert discusses. However, given the errors I find in his discussion of Avida, I am very dubious with respect to his analysis of the other programs. If he does so badly with something I know pretty well, why should I trust his judgement in areas I don’t know so well?

After repeating an introduction to Avida that I wrote some years ago, I will follow (roughly) Ewert’s analysis, in which he first describes all five programs and then criticizes them. Hence, I’ll look at Ewert’s description of Avida, and in particular note several errors in it, and then I’ll evaluate his criticisms. I find that his description is faulty and his critique ill-founded.

A Very Darwinian Halloween

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It’s Halloween, so it’s time for a roundup of the SCARIEST October stories in the evolution versus creationism wars!

Heh, five years later and Casey Luskin is still trying to refute the immune system cross: http://www.evolutionnews.org/2010/1[…]_042001.html

Never mind that Luskin’s one immunologist, Donald Ewert, admits that most of his colleagues, even his coauthors, are against him and use homology and comparative evidence everywhere all the time; admits that there is a mountain of literature on the evolution of the immune system; and admits (although he barely stammers it out) that there actually is an evolutionary model for the origin of receptor rearrangement in adaptive immunity and that the researchers themselves interpreted this as confirmation of the basic transposon-origins model (although Ewert somehow thinks this was just a “classification” of the RAG genes as bacterial transposons, ignoring, (a) how damned odd that is to find in vertebrate immune system genes and (b) how this was suspected ever since the 1970s and was deliberately tested in the 1990s-2000s).

Ewert’s reply basically boils down to vague denial of vast amounts of detailed work in evolutionary immunology, raw assertions that sequence similarity doesn’t suggest common ancestry (I dare Ewert/Luskin to do a survey of comparative immunologists on that point), and complaints about the literature not being detailed enough. Unfortunately for them, Behe made all these same points at trial. When you make these kinds of claims in the teeth of an entire specialized subfield which refutes you, it’s your credibility that’s shot, on the stand or anywhere else. So, try again. Give us a better, more detailed explanation of the origins of the immune system, Luskin and Ewert. Good luck!

I don’t have time to do a serious blog entry, but I would just note that Jerry Coyne has been blogging Behe’s QRB paper, and the scandalous abuse of it by ID proponents (well, I’m sure the abuse was intended by Behe, but what he could actually establish in a peer-reviewed paper does not support even a smidgen the claims that Behe and other ID fans are making about the paper on the blogs).

In the latest thread, Paul Nelson popped up with another promise for another piece explaining why something that’s obviously wrong is actually reasonable (in this case, why ID advocates are allowed to disdainfully ignore the massive evidence that gene duplication + divergence is the main source of new genes with new functions, and why they are allowed to claim that the origin of new functional sequence is a big problem, when in fact it’s basically a solved problem, with the answer – gene duplication + divergence – known across biology, tested and verified in numerous different ways, and written down for beginners in the textbooks). We’ll see if he ever comes up with it. But in the meantime, here are a few irate comments from me:

Apparently Behe has been mentioning this in his England tour:

Volume 85 Number 4 December 2010 Major Articles

Current Perspectives on the Biological Study of Play: Signs of Progress Kerrie Lewis Graham and Gordon M. Burghardt

Experimental Evolution, Loss-of-Function Mutations, and “The First Rule of Adaptive Evolution” Michael J. Behe

What is an Individual Organism?: A Multilevel Selection Perspective Henri J. Folse III and Joan Roughgarden

Irreducible Incoherence and Intelligent Design: A Look into the Conceptual Toolbox of a Pseudoscience Maarten Boudry, Stefaan Blancke, and Johan Braeckman

The Boudry article is online here and is quite good, catching points that most commentators on the IC argument miss. (Part of the goodness is that it cites Pete Dunkleberg’s 2003 “IC Demystified” at talkdesign.org, which is one of the better discussions out there.)

If past experience is any guide, Behe’s article will make abstract arguments about the improbability of adaptations *if* many simultaneous events are required, but will present no evidence that many simultaneous events are likely to be necessary for the sorts of adaptations we actually see in biology. Positive evidence for ID will not be provided at all, but the article will be trumpeted as such by the usual ID propagandists. But the article isn’t out yet, so we’ll see, I suppose.

There hasn’t been a heck of a lot to talk about regarding the ID movement lately. ID arguments have always been recycled creationist silliness, but in the early days, at least they would update the arguments to apply them to somewhat new/interesting systems, like the bacterial flagellum, and thus there would be something to talk about for awhile. But after the Kitzmiller case and followup publications in 2006-2007, pretty comprehensive rebuttals of all of the ID movement’s major arguments and attempted examples have been available.

Junker_Scherer_2009_edition6.jpgI just came across what is apparently a major online revision to the German creationist textbook Evolution - ein kritisches Lehrbuch, by Reinhard Junker and Siegfried Scherer. The section is section 9.4. There is an HTML summary (original German, google translation) and a 32-page PDF is here (apparently too long for google to translate).

Sadly, while I took German in high school, most of what I remember involves beer-drinking songs, which doesn’t help me out much here. Clearly Matzke (2003/6) and Pallen & Matzke (2006) and perhaps other commentary on flagellum evolution got deep under their skin – most of the chapter seems to be taken up with attempting to refute the evolutionary model for the origin of the flagellum! Regardless, I can tell there are a few issues – they cite the 2003 critiques of the flagellum evolution model by the pseudonymous “Mike Gene”, without noting that several later scientific developments caused Mike Gene to substantially improve his opinion about even the most radical part of Matzke 2003, which was the idea that a good chunk of the flagellum was homologous to the F1Fo-ATPase and relatives. (The original seems to be lost to the internet ghosts, but Ed Brayton blogged it, see: “Mike Gene Admits Matzke was Right”)

Anyway, if anyone knows of a source that can translate PDFs, or if there are any German speakers up for summarizing their main points, it would be interesting to hear if they’ve come up with anything new. I mean, there’s 32 whole pages, so maybe they will actually acknowledge that Luskin & numerous DI sources were wildly wrong about the number of required, flagellum-unique proteins in the flagellum. And actually, it does look kind of like Junker & Scherer are advancing some argument that relies on the idea that the flagellum parts are not unique, but instead were designed to serve multiple independent functions (see Figure 4). How conveniently like evolutionary cooption!

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.

Eppur si muove!

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Blogging on Peer-Reviewed Research

The Harvard multimedia team that put together that pretty video of the Inner Life of the Cell has a whole collection of videos online (including Inner Life with a good narration.) Go watch the one titled F1-F0 ATPase; it's a beautiful example of a highly efficient molecular motor, and it's the kind of thing the creationists go ga-ga over. It's complex, and it does the same rotary motion that the bacterial flagellum does; it has a little turbine in the membrane, a stream of protons drives rotation of an axle, and the movement of that axle drives conformation changes in the surrounding protein that promote the synthesis of ATP. It's a molecular machine all right. Makes a fellow wonder if possibly it's "irreducible", doesn't it?

Well, it's not. It can be broken down further and it still retain that rotary motion.

Continue reading "Eppur si muove!" (on Pharyngula)

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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.

Behe review in TREE

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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:

flunked.jpg

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.

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