Arthur Hunt Archives

Well that was interesting

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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.) 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 had expected.

I have posted a longer essay on my blog, where comments may also be made. I’ll summarize the most important points here, focusing just on the questions I was able to ask. Due to the time constraints, I only got to ask three questions. The answers and discussion that followed these included some interesting (and perhaps important) concessions. Briefly, Meyer did not offer to disagree with the notion that there are in some senses a disconnect between the quantity of specified information (in whatever sense he uses the term in his book - please refrain from rehashing this issue in the comments) and biological function. He also granted that some of the analogies he uses in his book were not really strong selling points for the design argument. (My question focused on the analogy with computers and engineered objects.) Finally, he intimated that high specified information content was not a feature of all proteins. This latter point may seem obvious, but I think it important to have ID advocates backing down from claims or even hints that all (or even most) proteins have high specified information contents.

That’s my experience in a very small nutshell. I would have liked more time for questions, to be sure. But in general the format that was proposed to me was followed. To be sure, Meyer danced around many of the issues, but in retrospect this may have been because I pressed him on things that he was not familiar with.

I haven’t tried to sum up Steve Matheson’s questions or impressions. I suspect that he will give his these on his blog. Stay tuned.

Signature in the Cell?

(The following is a follow-up to a comment I made in this thread.) 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.

For details, follow this link, where comments may be left.

This essay is the third of a series authored by Dave Wisker, Graduate Student in Molecular Ecology at the University of Central Missouri.

This series of essays counters common Intelligent Design/Creationist arguments against the fixation of the fusion that produced human chromosome 2. To recap briefly, ID/C’s argue that the fusion would have resulted in a chromosome with two centromeres, which would then be torn apart during meiosis. In “The Dicentric Problem” I explained how the presence of two centromeres does not necessarily interfere with proper segregation. ID/C’s also claim that heterozygotes for the fusion suffer from greatly reduced fertility, preventing the fusion from ever becoming fixed. I explained how this is not true for centric fusions in “The Fertility Problem” . Using realistic values for human populations, “Fixation Within a Deme” showed that the fixation probability of the fusion within a local breeding population, or deme, may be between 4.5 and 10 percent. This final essay will look at the probability of fixation for the fusion in the species as a whole.

Lande (1979) looked at the problem of fixation for chromosomal rearrangements with heterozygote disadvantage. He constructed a model with populations subdivided into numerous, semi-isolated subpopulations, or demes, in which spontaneous chromosome rearrangements with heterozygote disadvantage occur. In addition, the model included random extinction and colonization of demes. Lande did not include mechanisms like meiotic drive (see “Fixation Within a Deme” for explanation) in his model, letting genetic drift (i.e., chance) be the primary force for fixation within a deme. He found that the biggest obstacle to overall fixation was establishment of the fusion within one deme. The overall fixation probability turned out to be the probability of fixation within that first deme:

Once established in a deme, a negatively heterotic [one with a selective disadvantage for heterozygotes–DW] gene arrangement can spread in homozygous form through a subdivided population by random local extinction and colonization. For this process, the fixation rate in a species composed of many semi-isolated demes is approximately equal to the rate of establishment of new gene arrangements in a single one of its demes.

In “Fixation Within a Deme”, I showed that meiotic drive plays a major role in influencing fixation of centric fusions in humans. In addition, the probable structure of early human populations is very similar to that used in Lande’s model. It is therefore reasonable to suggest the overall fixation probability for the human chromosome 2 fusion is at least the value of 4.5 -10% determined earlier.

Interestingly, there may be another factor that influenced the rise in frequency of human chromosome 2. Hedrick and Levin (1984) suggested a mechanism that greatly increases the probability of fixation for negatively heterotic chromosome rearrangements during migration and colonization of other demes. They pointed out that the process of colonization often involves small groups of individuals, so genetic drift in the form of the “founder effect” plays an important role. Furthermore, the individuals in these founder groups may be closely related. So, if a chromosome rearrangement becomes established in a deme, then any founder groups derived from it will already have the rearrangement at a very high frequency to start with. If the group establishes itself in an unoccupied area, fixation would be instantaneous for that deme. If the group joins another existing group, given that most demes are small, the newcomers may compose a significant percentage of the combined deme. Therefore, the initial frequency of the rearrangement could already be high enough to exceed the unstable equilibrium frequency (see “Fixation Within a Deme” for discussion of this) and thus drive the rearrangement to fixation there as well. Hedrick and Levin called this “kin-founding”. They note that kin-founding is common in many groups of organisms. Anthropological data confirms this in humans (Fix, 1978). Since Lande’s model does not incorporate mechanisms that influence fixation such as meiotic drive and kin-founding, there is reason to believe that the overall fixation probability for human chromosome 2 may be higher than the base calculation for the deme.

In conclusion, this series of essays effectively counters every ID/C claim about the probability of fixation of human chromosome 2, using actual data from human populations as well as population models based on plausible assumptions. It is up to the ID/C community to present data that specifically supports their contentions.

Many thanks to Art Hunt for discussions and publishing help, and the PT crew for encouragement. Many thanks also to the ID proponent ‘Ilion’ (wherever he may be) for getting me mad enough to actually put it all together.

References

Fix AG (1978). The role of kin-structured migration in genetic microdifferentiation. Ann. Hum. Genet. Lond. 41: 329-339.

Hedrick PW & DA Levin (1984). Kin-founding and the fixation of chromosomal variants. Amer. Nat. 124(6): 789-787

Lande R (1979). Effective deme sizes during long-term evolution estimated from rates of chromosomal rearrangement. Evolution 33(1): 234-251.

This essay is the third of a series authored by Dave Wisker, Graduate Student in Molecular Ecology at the University of Central Missouri.

In previous essays in this series, I have discussed two issues with the fusion that resulted in human chromosome 2: its dicentric nature, and the fusion’s possible effect on fertility. I showed how one extra centromere may not result in inevitable damage to the chromosome during meiosis and mitosis, and demonstrated that the fusion did not necessarily have to result in greatly decreased fertility. Either of those situations would have effectively prevented the fusion from rising in frequency and eventually becoming fixed in the human population. We are now in the position to consider the probability of such a fusion becoming fixed. This essay will examine the fixation probability of the fusion in a small subpopulation, or deme.

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.

This essay is the second of a series authored by Dave Wisker, Graduate Student in Molecular Ecology at the University of Central Missouri.

As I wrote in the previous essay in this series, Intelligent Design advocate Casey Luskin doesn’t think the fusion which produced human chromosome 2 could have become fixed in the human population:

Miller may have found good empirical evidence for a chromosomal fusion event. But our experience with mammalian genetics tells us that such a chromosomal aberration could have created a non-viable mutant, or a normal individual who could not produce viable offspring. Thus, Neo-Darwinism has a hard time explaining why such a random fusion event was somehow advantageous.

Luskin (and other ID/creationist apologists I’ve seen on internet discussion fora) maintain that the fusion which resulted in human chromosome 2 must have had drastic negative effects on the fertility of heterozygotes for the fusion. This reduction in fitness, they argue, would effectively prevent the propagation of the fusion throughout the population. On the surface, this sounds like an effective argument, since it is known that translocations and fusions can have such a negative effect by producing non-balanced gametes (see PZ Myers’s article on his blog Pharyngula for a detailed explanation). However, anyone familiar with the cytogenetic literature of mammals knows that one cannot claim that these rearrangements greatly decrease fertility with any certainty, since there are numerous examples where such an expected reduction does not occur.

This essay is the first of a series authored by Dave Wisker, a Graduate Student in Molecular Ecology at the University of Central Missouri.

Back in 2005, Casey Luskin wrote an article criticizing Kenneth Miller’s testimony at the Dover ID trial called “And the Miller Told His Tale: Ken Miller’s Cold (Chromosomal) Fusion”. Luskin took Miller to task for showing that the chromosomal fusion which resulted in human chromosome 2 was evidence for the common ancestry between humans and the great apes. His argument was ably taken apart by PZ Myers here and Mike Dunford here.

Luskin also wrote:

In other words, Miller has to explain why a random chromosomal fusion event which, in our experience ultimately results in offspring with genetic diseases, didn’t result in a genetic disease and was thus advantageous enough to get fixed into the entire population of our ancestors. Given the lack of empirical evidence that random chromosomal fusion events are not disadvantageous, perhaps the presence of a chromosomal fusion event is not good evidence for a Neo-Darwinian history for humans.

Both Myers and Dunford pointed out those heterozygotes for the type of chromosomal fusion in question did not necessarily have to suffer from genetic disease or infertility. But they did not discuss the plausibility of the fixation of the fusion in the human population. In a series of forthcoming essays I will examine this, and also address some other common ID/creationist ‘problems’ with the fusion not mentioned by Luskin. The first problem is:

The Dicentric Problem

In an earlier essay, I argued that the process(es) by which symbionts become organelles constitute macroevolutionary change. While this was discussed largely in the context of a fascinating long-term experiment begun by K. W. Jeon and colleagues in the 1960’s, it is also relevant to the origins of more identifiable organelles such as mitochondria and chloroplasts. Which brings me to another matter, a line of experimentation that shows yet another case whereby macroevolutionary change can be studied by direct experimentation, almost in real time.

The progression from symbiont to organelle involves many steps or processes. Among these is a migration of genes from the symbiont genome to the host genome. The end results of such migrations may be seen in the genomes of modern eukaryotes; thus, nuclear genomes are “littered” with genes that are derived from prokaryotic ancestors, but are expressed as eukaryotic genes and whose protein products end up in the organelle. Attendant with such migrations have been a number a number of changes, modifications that would permit the new nuclear gene to be expressed, and its protein product to be transported from the cytoplasm into the organelle.

Until recently, studies of these migrations have been matters of sequence comparisons and analyses. These approaches are very informative, and have told us about the ancestry of the relevant genes. However, for the most part, matters of mechanism have been harder nuts to crack, largely because it had been assumed that migratory events occur on an evolutionary time scale, and thus that they would be unlikely to be caught “in the act”. Recent studies reveal that this is not the case. Briefly, it is now known that gene migration from organelle to nucleus can be observed and studied in real time, and that questions pertaining to the “activation” of organellar genes after migration to the nucleus can be asked (and answered). In other words, this sort of macroevolutionary change can be studied as it occurs.

There is more to this story, some of which may be found here, where comments may also be left. (As a further teaser, I would note that this phenomenon impacts the field of biotechnology and GMOs.) The bottom line is simple, though - macroevolutionary changes involving gene migration can be studied in real time, once again putting the lie to the ID/antievolutionist assertion that macroevolution cannot be addressed experimentally.

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.

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.

(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.).

In previous essays (here and here), we learned that genes encoding new proteins can and do, often, arise de novo in the course of evolution, contradicting one of the central tenets of ID proponents. The means by which these genes arise are many. One of these, suggested by Cai at al. (the subject of one of the earlier essays), involved the adaptation of a gene encoding an evolutionarily-conserved non-coding RNA via the appearance, by mutation, of appropriate translation initiation and termination (“start” and “stop”) codons. This mechanism represents an intersection of sorts between the subject of protein evolution and another matter of discussion on these blogs, namely the existence, evolution, and “function” of junk DNA. In this essay, I review a 2007 study by Debrah Thompson and Roy Parker (“Cytoplasmic decay of intergenic transcripts in Saccharomyces cerevisiae”, Mol. Cell. Biol. 27, 92-101) that adds a great deal of clarity to this mode of gene and protein evolution.

Recently, we learned of an instance of the de novo origination of a new protein-coding gene in yeasts. This instance involved a mechanism or pathway that seems difficult to some, namely the random appearance of an open reading frame in an otherwise noncoding segment of DNA via judicious appearance of translation start and stop codons. The question naturally arises as to the relevance of such a pathway to real-life biology; was/is this a rather rare event that doesn’t really contribute to protein evolution, or is it a common means by which the protein-coding capacity of a genome is augmented?

A paper that is in press in Genome Research (Zhou et al., “On the origin of new genes in Drosophila”) gives us some insight into this question. The abstract of this paper summarizes things as well as I can:

A recurrent theme amongst ID proponents is the supposed difficulty of protein evolution, especially as it relates to the origination of new protein-coding genes. This is, I suspect, a key reason why ID proponents such as Paul Nelson are so enamoured of ORFans, and a foundational principle for the application of ID theory to evolution (the idea being that protein-coding genes are possessed of Complex Specified Information, and thus cannot arise by natural processes). Thus, studies that pertain to the origins of new protein-coding genes are going to factor largely in the scientific aspect of the ID debate, especially since ID proponents insist that new protein-coding genes cannot arise “by chance”.

It is in this context that a recent study by Jing Cai and colleagues is of interest. The title of the article suffices to explain the study – “De novo Origination of a New Protein-Coding Gene in Saccharomyces cerevisiae”. What these authors describe is a series of studies of a yeast gene, BSC4. This gene was originally identified as a candidate containing a so-called read-through translation termination (or stop) codon. This gene was studied in more depth, whereupon Cai et al. found that the protein encoded by this gene was novel in genome databases, not resembling any other protein in any organism. Importantly, this includes the genomes of related Saccharomyces species; this indicates that this protein in S. cerevisiae arose relatively recently, after this species diverged from its close relatives.

Junk to the second power

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The ID blogosphere is much agog, and has been for some time, about recent (and not so recent) results that suggest some sort of functionality in what has long considered to be nonfunctional (junk) DNA in eukaryotes. The most recent buzz centers on studies (such as ENCODE ) that indicate that large swaths of so-called junk DNA are “expressed” by RNA polymerase II. Apparently, the fact that RNA polymerase transcribes alleged junk DNA is a blow to Darwinism, and a feather in the cap of ID. Their excitement in this regard, I suspect, will wane greatly once they learn some of the true implications of these results. For the matter of “expression” in junk DNA is one wherein ID meets, and gets swallowed by, the Garbage Disposal.

What follows is a discussion of a relatively recent report that rains on the ID parade. As is my habit, I’ll summarize the essay for those with short attention spans – the bottom line is that the so-called “function” that so excites the ID proponents may be little more than manifestations of quality control in gene expression, and that the supposed functional swaths of non-coding junk DNA may be nothing more than parts of the genome that encode, and lead to the production of, “junk” RNA (if I may so bold as to coin a phrase). In a nutshell, junk piled on top of junk.

In biology, genetics, biochemistry, and molecular biology classes, one of the things that we used to learn that distinguishes prokaryotes from eukaryotes is the “fact” that eukaryotes have polyadenylated mRNAs, while prokaryotes do not. This morphed rather easily into a distinction – eukaryotes do polyadenylation, prokaryotes do not. For years, this was standard fare in class. However, even as generations of students (beginning with the discovery of polyadenylate tracts in hnRNA in eukaryotes) were learning of this distinction, we knew that all was not right with this. Among the lurking pieces of conflicting data was that the first biochemical entity that was shown to add poly(A) tracts to RNAs in vitro was a bacterial one, isolated and purified from E. coli (1).

Reality 1, Behe 0

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Or …

T-urf13 redux

A few months ago I posted an essay about a remarkable example of the evolution of Irreducible Complexity from scratch, via natural, unguided mechanisms. While the reaction to this essay has been pretty muted (precious little to take note of, save for one well-hidden reference on Uncommon Descent to “No Free Lunch”, citing pages that make arguments clearly refuted in the PT essay), I had no idea that a much bigger response, or target, would emerge from the Halls of ID. This would, of course, be Mike Behe’s recently-released follow-up to “Darwin’s Black Box”, entitled “The Edge of Evolution”.

More follows beneath the fold, but here’s the short version for those of us with miniscule attention spans -the previous essay refutes (or, better said, refuted) the EoE in no uncertain terms, showing that the centerpiece of the EoE, the value Behe assigns to the “probability” of occurrence of a protein interaction or binding site, does not agree with what we can and do know about the history of a bonafide multiple simultaneous mutation.

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.

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.

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