ERV alerted me to Luskins latest attempt to, well, um, I’m not sure what because all he succeeds in doing is undermining several ID talking points. ERV tackles Luskin’s post in her own inimitable style (linked to above) but I would like to focus on a couple of other points – especially the one where he throws Behe under the bus.
The subject of Luskin’s post concerns “junk” or noncoding DNA:
These sources promoting the classic “junk DNA” icon of neo-Darwinism need updating, as a Yale University news release from earlier this month recalls the fact that “[i]n the last several years, scientists have discovered that non-coding regions of the genome, far from being junk, contain thousands of regulatory elements that act as genetic ‘switches’ to turn genes on or off.” In this case, the junk triggered genes that control human thumb and foot development.
Luskin is being more than a little dishonest here, since, as I have previously pointed out there are a number of competing explanations for noncoding DNA. Note also Luskin’s description of the function of this junk. Is this really such a radical discovery that it is going to challenge evolutionary science? Well, no. This is actually another example of Luskin making ad hoc arguments simply because they contradict evolutionary theory. In accepting the results of this paper – that this particular DNA has a function – Luskin has given the farm away. To understand why we need to look at the paper in more detail. The paper in question is called Human-Specific Gain of Function in a Developmental Enhancer and was published in Science on 9/5/08. There are a number of evolutionarily conserved noncoding DNA in vertebrate genomes. This paper picks the most rapidly evolving bit from the human genome. Compared to other vertebrates this particular bit (which the authors named HACNS1) has 16 human specific substitutions which were picked up after the human-chimp divergence. To try and understand the function of HACNS1 the researchers inserted the human version and the chimp and rhesus orthologs into a transgenic mouse enhancer assay (I’ll spare you the details) and looked at the resulting patterns of expression. They looked at embryos at two different stages of development (embryonic days 11.5 and 13.5). At day 11.5 the human HACNS1 was strongly expressed in the anterior limb bud, pharyngeal arches, and the ears and eyes. In contrast, the chimp and rhesus orthologs were only weakly expressed at the base of the limb. At day 13.5 the human HACNS1 was expressed in the forearm/hand junction, shoulder, and hindlimb. The chimp and rhesus orthologs showed expression in the shoulder region. The authors conclude:
These results indicate that the human-specific enhancer activity persists across multiple developmental stages. Moreover, they suggest that the robust anterior limb expression pattern of HACNS1 evolved from a weaker ancestral pattern that is largely confined to the base of the limb bud, as evident in the activities of the chimpanzee and rhesus enhancers at both time points.
Indeed, if one looks at the fossil record beginning with the chimp-human split and moving forward, one can see changes in exactly those structures HACNS1 is expressed in, which gives some robust support to the idea (IMHO). Having said that, I should also point out that although HACNS1 has a role to play in the evolution of the human skeleton, I doubt that it is the only cause. At any rate, if one accepts that HACNS1 has a function, one has to accept that the differences between chimps and humans arose as the result of human evolution. To argue otherwise would be illogical in the extreme. Luskin, of course, mentions none of this because to do so would put him between a rock and a hard place.
Luskin’s position becomes even more precarious when Prabhakar et al 2008 start talking about their reasoning for choosing this region. According to Prabhakar et al 2008, this region has undergone several bouts of positive selection that resulted in the function Luskin invokes. All quite interesting, but I’m sure you want to hear about Luskin throwing Behe under the bus. Here is what happened. The above experiments with human HACNS1 and its chimp and rhesus orthologs clearly demonstrate that anywhere from 1-16 of the human specific changes are responsible for the change or gain in function. Thirteen of the changes were tightly clustered in one area so Prabhakar et al 2008 focused on those. The inserted various combinations of six and three substitutions. The upshot is that at least two of the substitutions are required for the change in function – something Behe says can’t happen. It get’s somewhat worse though, because this work demonstrates that human evolution is mosaic evolution, irreducible complexity doesn’t apply.
PvM at the Panda’s Thumb offers his take on Luskin’s silliness as well.
Shyam Prabhakar, Axel Visel, Jennifer A. Akiyama, Malak Shoukry, Keith D. Lewis,
Amy Holt, Ingrid Plajzer-Frick, Harris Morrison, David R. FitzPatrick, Veena Afzal,
Len A. Pennacchio, Edward M. Rubin, James P. Noonan 2008 Human-Specific Gain of Function in a Developmental Enhancer, Science 321:1346-1350