Casey Luskin is doing a series of posts at the DI blog alleging to show “international scientific discoveries” since the Dover ruling that “support ID.” Given the long history of ID advocates claiming that some research project supports ID when it really doesn’t, one obviously expects more of the same here; one won’t be disappointed. In the first post in the series, for example, he actually admits that the DI’s new Biologic Institute labs will be doing research just like Douglas Axe’s 2000 Journal of Molecular Biology paper:

Biologic scientist Doug Axe has done much work assessing the probability of constructing functional proteins, which New Scientist reports was published in the Journal of Molecular Biology. The New Scientist article explains that ID proponents use the research to argue that “[b]ecause such mutations destroy ‘the possibility of any functioning’ in the enzyme, it could not have arisen via ‘Darwinian pathways’.”

Well yes, ID proponents do use the research to argue that, but only by rather boldly lying about what it says. This nonsense about Axe’s paper and how it allegedly supports ID has become a mantra for the ID folks, presumably practiced in a mirror over and over again until it can be said with a straight face. Indeed, Luskin uses a phrase virtually identical to the one used by William Dembski to describe Axe’s 2000 paper:

But there is now mounting evidence of biological systems for which any slight modification does not merely destroy the system’s existing function, but also destroys the possibility of any function of the system whatsoever (see Axe 2000). For such systems, neither direct nor indirect Darwinian pathways could account for them.

It’s an astonishing statement, really. He is claiming that Axe’s paper supports the claim that the biological system he studied (in this case, a particular enzyme) were so sensitive to any mutation that any slight modification would not only destroy the system’s existing function but would even destroy the possibility of any function whatsoever. This description of the results of Axe’s experiment could not be more inaccurate if it was designed intentionally to deceive people (and it was).

Matt Inlay shredded this claim at the Panda’s Thumb almost two years and no ID advocate, to my knowledge, has ever attempted to dispute what he wrote then. Here’s the truth about Axe’s paper. Axe took an enzyme and made amino acid substitutions in the exterior residues in the sequence. He did these substitutions in sets of 10 at a time, something that would be quite rare in nature where a point mutation would only change a single amino acid. He had 4 sets of 10 substitutions (the equivalent of 10 point mutations in nature) that he induced in the lab and found that none of the 4 sets of 10 substitutions had a significant effect on the enzyme’s function.

In fact, he had to combine three sets of 10, or 30 amino acid substitutions, in order to reduce the enzyme’s function by 99%, and had to combine all four, or 40 substitutions, in order to kill the function completely. 40 subsitutions accounted for 10% of the total amino acids in the enzyme, and a full 20% of the enzyme’s exterior residues. Does knocking out 20% of the amino acids before destroying function really sound like “any slight modification” to you? This would be nearly impossible in nature, requiring 40 separate mutations all at the same time.

What this research really shows, of course, is that small modifications in a protein, such as those brought on by point mutations that result in precisely this kind of amino acid substitution, can and do have a marginal effect on the protein’s function. If a single mutation results in a small increase in the ability of that protein to perform its function (say, binding to oxygen molecules or to invading bacteria), that may well be enough for that mutation to be selected for and to become fixed in the genome of that organism.

That is precisely what evolution requires and predicts and it is exactly what Axe’s experiment found. There is absolutely nothing in that study that supports ID or that questions evolution in any way. And in fact, it gets even worse for these claims. Remember, Dembski’s claim was not only that these “slight modifications” destroyed the protein’s function but also destroyed “the possibility of any function whatsoever.” But as Matt Inlay pointed out, Axe did not attempt to test for other possible functions, only for its original function. But others have, and here’s what they found:

However, as it turns out, another group analyzed mutations in the active site of the exact same gene (TEM-1) and found that certain “slight modifications” drastically reduced the original function of the system (penicillin and ampicillin resistance), but increased a separate, distinct function (cephalosporin resistance).

So what does this mean? It means that in certain environments, where the bacteria was under attack not by penicillin or ampicillin but by cephalosporin, the mutations that were induced in that particular experiment would actually be beneficial to the organism by increasing its resistence to the very substance attacking it. All of this is strong confirmation of the notion that mutations do not merely have to increase a protein’s existing function, but can result in a change in function that might aid in survival. Again, exactly what evolution expects.

No only does the Axe paper not support ID, it strongly supports evolutionary theory on multiple levels. And Luskin says that the Biologic Institute, where Axe is now the head researcher, is going to turn out more of the same. We knew that already, of course, but it’s nice to see it confirmed. And as further evidence, Luskin points to yet another bit of research that doesn’t support ID no matter how much he wishes it would:

Research from other labs is showing that evolving functional complexes of proteins may be difficult. A recent Nature paper finds that the intolerance of proteins to random mutations is heightened when that protein is part of a suite of interacting proteins: “the combined deleterious effects of mutations were, on average, larger than expected from the multiplication of their individual effects.”

Ironically, this paper involves the exact same enzyme (TEM-1) that Axe worked on in the above paper. And here’s what the study concludes, according to the abstract:

Subjecting TEM-1 to random mutational drift and purifying selection (to purge deleterious mutations) produced changes in its fitness landscape indicative of negative epistasis; that is, the combined deleterious effects of mutations were, on average, larger than expected from the multiplication of their individual effects. As observed in computational systems, negative epistasis was tightly associated with higher tolerance to mutations (robustness). Thus, under a low selection pressure, a large fraction of mutations was initially tolerated (high robustness), but as mutations accumulated, their fitness toll increased, resulting in the observed negative epistasis.

In other words, lots and lots of accumulated mutations has a much larger effect on the function of this enzyme than smaller numbers of accumulated mutations, and the more mutations accumulate, the faster the effects on function increase. If your reaction to that conclusion is along the lines of “well duh”, that would be a reasonable reaction. This is hardly a shocking development, nor does it provide any support for ID whatsoever.

The ID advocates know this, of course, but more importantly they know that the vast majority of their followers and financiers don’t know this and aren’t the least bit interested in it anyway. And that’s why this pattern of vastly overclaiming, or even outright lying, about the results of various bits of research continues to go on and is unlikely to stop. They may not be able to fool all of the people all of the time, but they don’t need to.