I do enjoy reading ID’s most vehement critics, both in formal publications (such as books and papers) and on the, somewhat less formal, Internet blogosphere. Part of the reason for this is that it gives one something of a re-assurance to observe the vacuous nature of many of the critics’ attempted rebuttals to the challenge offered to neo-Darwinism by ID, and the attempted compensation of its sheer lack of explicative power by the religious ferocity of the associated rhetoric (to paraphrase Lynn Margulis). The prevalent pretense that the causal sufficiency of neo-Darwinism is an open-and-shut case (when no such open-and-shut case for the affirmative exists) never ceases to amuse me.
One such forum where esteemed critics lurk is the Panda’s Thumb blog. A website devoted to holding the Darwinian fort, and one endorsed by the National Center for Selling Evolution Science Education (NCSE). Since many of the Darwinian heavy guns blog for this website, we can conclude that, if consistently demonstrably faulty arguments are common play, the front-line Darwinism defense lobby is in deep water.
Recently, someone referred me to two articles (one, two) on the Panda’s Thumb website (from back in 2007), by Arthur Hunt (professor in Department of Plant and Soil Sciences at the University of Kentucky). The first is entitled “On the evolution of Irreducible Complexity”; the second, “Reality 1, Behe 0” (the latter posted shortly following the publication of Behe’s second book, The Edge of Evolution).
The articles purport to refute Michael Behe’s notion of irreducible complexity. But, as I intend to show here, they do nothing of the kind!
In his first article, Hunt begins,
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).
There is no need to discuss the cited Long et al. (2003) paper in any great detail here, as this has already been done by Casey Luskin here (see also Luskin’s further discussion of Anti-Freeze evolution here), and I wish to concern myself with the central element of Hunt’s argument.
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.
Hunt is making big promises. But does he deliver? Let me briefly summarise the jist of Hunt’s argument, and then briefly weigh in on it.
The cornerstone of Hunt’s argument is principally concerned with the gene, T-urf13, which, contra Behe’s delineated ‘edge’ of evolution, is supposedly a de novo mitochondrial gene that very quickly evolved from other genes which specified rRNA, in addition to some non-coding DNA elements. The gene specifies a transmembrane protein, which aids in facilitating the passage of hydrophilic molecules across the mitochondrial membrane in maize – opening only when bound on the exterior by particular molecules.
The protein is specific to the mitochondria of maize with Texas male-sterile cytoplasm, and has also been implicated in causing male sterility and sensitivity to T-cytoplasm-specific fungal diseases. Two parts of the T-urf13 gene are homologous to other parts in the maize genome, with a further component being of unknown origin. Hunt maintains that this proves that this gene evolved by Darwinian-like means.
Hunt further maintains that the T-urf13 consists of at least three “CCCs” (recall Behe’s argument advanced in The Edge of Evolution that a double “CCC” is unlikely to be feasible by a Darwinian pathway). Two of these “CCCs”, Hunt argues, come from the binding of each subunit to at minimum two other subunits in order to form the heteromeric complex in the membrane. This entails that each respective subunit have at minimum two protein-binding sites.
Hunt argues for the presence of yet another “CCC”:
[T]he ion channel is gated. It binds a polyketide toxin, and the consequence is an opening of the channel. This is a third binding site. This is not another protein binding site, and I rather suppose that Behe would argue that this isn’t relevant to the Edge of Evolution. But the notion of a “CCC” derives from consideration of changes in a transporter (PfCRT) that alter the interaction with chloroquine; toxin binding by T-urf13 is quite analogous to the interaction between PfCRT and chloroquine. Thus, this third function of T-urf13 is akin to yet another “CCC”.
He also notes that,
It turns out that T-urf13 is a membrane protein, and in membranes it forms oligomeric structures (I am not sure if the stoichiometries have been firmly established, but that it is oligomeric is not in question). This is the first biochemical trait I would ask readers to file away – this protein is capable of protein-protein interactions, between like subunits. This means that the T-urf13 polypeptide must possess interfaces that mediate protein-protein interactions. (Readers may recall Behe and Snokes, who argued that such interfaces are very unlikely to occur by chance.)
Hunt tells us that “the protein dubbed T-urf13 had evolved, in one fell swoop by random shuffling of the maize mitochondrial genome.” If three CCC’s really evolved in “one fell swoop” by specific but random mutations, then Behe’s argument is in trouble. But does any of the research described by Hunt make any progress with regards to demonstrating that this is even plausible? Short answer: no.
Hunt does have a go of guesstimating the probabilistic plausibility of such an event of neo-functionalisation taking place. He tells us, “The bottom line – T-urf13 consists of at least three ‘CCCs’. Running some numbers, we can guesstimate that T-urf13 would need about 10^60 events of some sort in order to occur.”
Look at what Hunt concludes:
Now, recall that we are talking about, not one, but a minimum of three CCC’s. Behe says 1 in 10^60, what actually happened occurred in a total event size of less that 10^30. Obviously, Behe has badly mis-estimated the “Edge of Evolution”. Briefly stated, his “Edge of Evolution” is wrong. [Emphasis in original]
Readers trained in basic logic will take quick note of the circularity involved in this argumentation. Does Hunt offer any evidence that T-urf13 could have plausibly evolved by a Darwinian-type mechanism? No, he doesn’t. In fact, he casually dismisses the mathematics which refutes his whole argument. Here we have a system with a minimum of three CCCs, and since he presupposes as an a priori principle that it must have a Darwinian explanation, this apparently refutes Behe’s argument! This is truly astonishing argumentation. Yes, certain parts of the gene have known homologous counterparts. But, at most, that demonstrates common descent (and even that conclusion is dubious). But a demonstration of homology, or common ancestral derivation, or a progression of forms is not, in and of itself, a causal explanation. Behe himself noted in Darwin’s Black Box, “Although useful for determining lines of descent … comparing sequences cannot show how a complex biochemical system achieved its function—the question that most concerns us in this book.” Since Behe already maintains that all life is derivative of a common ancestor, a demonstration of biochemical or molecular homology is not likely to impress him greatly.
How, then, might Hunt and others successfully show Behe to be wrong about evolution? It’s very simple: show that adequate probabilistic resources existed to facilitate the plausible origin of these types of multi-component-dependent systems. If, indeed, it is the case that each fitness peak lies separated by more than a few specific mutations, it remains difficult to envision how the Darwinian mechanism might adequately facilitate the transition from one peak to another within any reasonable time frame. Douglas Axe, of the biologic institute, showed in one recent paper in the journal Bio-complexity that the model of gene duplication and recruitment only works if very few changes are required to acquire novel selectable utility or neo-functionalisation. If a duplicated gene is neutral (in terms of its cost to the organism), then the maximum number of mutations that a novel innovation in a bacterial population can require is up to six. If the duplicated gene has a slightly negative fitness cost, the maximum number drops to two or fewer (not inclusive of the duplication itself). One other study, published in Nature in 2001 by Keefe & Szostak, documented that more than a million million random sequences were required in order to stumble upon a functioning ATP-binding protein, a protein substantially smaller than the transmembrane protein specified by the gene, T-urf13. Douglas Axe has also documented (2004), in the Journal of Molecular Biology, the prohibitive rarity of functional enzymatic binding domains with respect to the vast sea of combinatorial sequence space in a 150 amino-acid long residue (Beta-Lactamase).
What, then, can we conclude? Contrary to his claims, Hunt has failed to provide a detailed and rigorous account of the origin of T-urf13. Hunt also supplies no mathematical demonstration that the de novo origin of such genes is sufficiently probable that it might be justifiably attributed to an unguided or random process, nor does he provide a demonstration that a step-wise pathway exists where novel utility is conferred at every step (being separated by not more than one or two mutations) along the way prior to the emergence of the T-urf13 gene.
The Panda’s Thumb are really going to have to do better than this if they hope to refute Behe!