A Review Of Sean Carroll's Presentation: 'Revisiting The Forensic Record Of Evolution'
By Robert Deyes
Last month forensic scientists from all over the world convened in Hollywood for the 19th Annual Symposium On Human Identification. Notable amongst the talks was that of keynote speaker, molecular biologist Sean Carroll who kicked off the proceedings with a much anticipated presentation on how DNA had impacted our understanding of the evolution of life. One by one, he covered several examples that he claimed supported the purposeless meanderings of the Darwinian process.
First on Carroll's list was the ice fish- a rather curious creature that lives in the southern ocean close to Antarctica. For years scientists have puzzled over the finding that the blood of the ice fish is completely colorless- a feature not seen in any other living vertebrate. It turns out that only 1% of ice fish blood is actually made up of cells, a far cry from, say, the 40% cell content of human blood. What evolutionary advantage could be gained from fewer cells to carry the nourishment so vital for survival? Carroll argued that such a low cell content represented a key adaptation to the cold environment of the Antarctic waters. So the story goes, by carrying fewer cells, the resulting lower-viscosity blood could continue to flow even with the bitterly cold sea temperatures. The ice fish had seemingly evolved to withstand the harsh realities of its environment. Carroll turned to DNA evidence in support of his inference. While all other fish have two globin genes- alpha1 and beta globin- it turns out that ice fish carry a partly-deleted copy of alpha1 and lack the beta globin gene altogether. These deletions, Carroll commented, are inextricably linked to its lower blood viscosity and have seemingly produced a key adaptation in the ice fishes' fight for survival. Moreover, the ice fish carries a suite of anti-freeze proteins that, Carroll asserted, were co-opted from other proteins to suppress the growth of dangerous ice crystals in its gills.
Carroll's rendition of nature's ways continued unabated with his proclamation that the skin color of the Rock Pocket mouse in the Panacate lava flow of Arizona had similarly evolved in response to environmental cues. The foundations of this adaptation had everything to do with a gene called MCIR. It turns out that mice living on the dark larval soils of Panacate carry a 'dark' MCIR gene, hence their dark coat. Conversely the mice living on sand-colored soils carry a 'light' gene that gives them their characteristic sand-color. Once again Carroll gave the purposeless hand of evolution full credit for these differences, with variation by random mutation playing the lead role in bringing forth key evolutionary adaptations. And yet problematic for Carroll was the lack of a viable explanation for how genes such as MCIR as well as alpha1 and beta globin had arisen 'de novo' through natural processes (Ref 1). There was no evidence from the examples given that natural selection could do anything other than tinker with already-existing genetic information. Mutation and degradation, rather than construction and assembly, were words that Carroll used often during his discourse. As for his claims on co-opted proteins, one was left with the question of how mechanistically proteins could mutate and end up in just the right place elsewhere within the organismal 'milieu' to fulfill novel functions. As biochemist Michael Behe succinctly summarized, active proteins would be "ill suited for virtually any new role" (Ref 2, p. 66).
Resurrecting the iconic status of the deep sea coelacanth, Carroll went on to describe this creatures' inability to see in color, citing the degradation of a series of genes called opsins as the root cause of its visual deficiencies. So the story goes, since color was no longer discernible in the deepest recesses of our oceans, selective pressure to maintain color-seeing opsins in the coelacanth was no longer operational. By the same token, mutations in opsins appear to have given rise to the European kestrel's ability to visualize the UV reflection of rodent urine, providing it with important clues on the location of its prey. The same sort of reasoning lay behind the loss of functionality in the opsin genes of other animals such as the red-eyed owl monkey, the subterranean bush-baby and the blind vole rat. Indeed the 'use it or lose it' nature of these so-called fossil genes became Carroll's argument against intelligent design. After all, what designer in his right mind would place a multitude of non-functional genes into a genome?
Carroll's argument against design eschewed the real question of how genes came into existence through natural processes. There are no grounds for assuming that the processes through which genes might degrade are the same processes through which they could be built up (Ref 1). In simple terms, genes are long stretches of DNA that carry the information necessary to code for the production of functional proteins. Intelligent design theorists claim that a piece-meal assembly of information-rich genes using the basic building blocks of DNA exceeds the capacities of Darwinian selection and is better explained by appealing to the activity of an intelligent agent (Refs 3,4). If anything, this very principle should have been Carroll's first point of contention if he was to say anything against ID. From a philosophical perspective the possibility remains that a designer may have supplied an organism with more genetic information than may have been needed for life- what one may call an "all the options, all the bells and whistles" approach. Such a designer could have been interested in placing non-functional genes in the genome for a future role in his or her design. We all install software into our computers that may not be operational until some later date when we finally choose to use it. Computers can now be accurately scheduled to start a process at a specified instant in the future, similarly to the programming of a recording on a video-recorder.
One may rightly ask what evidence Carroll could furnish to support the premise that non-functional genes were necessarily derived from functional counterparts found elsewhere in nature. Indeed empirical evidence in support of an evolutionary continuum was severely lacking throughout the presentation. To be fair, Carroll did inject some much needed humor by showing a short clip of Aardman Animations' 'Creature Comforts On Evolution'. The images of talking animals explaining their evolutionary origins were received amidst bouts of laughter from the audience. And yet Carroll was unable to buttress up his non-design inference with any objective data. Indeed one can only imagine how things might have turned out if Intelligent Design supporters had been invited to present their side of the argument. In such a scenario, Carroll's case for fossil genes might have been shown to be nothing more than fossilized rhetoric.
1. A key point about the loss of function mutations is that no additional genetic sequences, and therefore no additional information, has been added to the gene involved. In his book 'Not By Chance', Lee Spetner notes how for the grand sweep of evolution to occur, information has to be built up.
2. Michael J Behe (1996), Darwin's Black Box-The Biochemical Challenges to Evolution 1st Edition Published by Simon and Schuster, New York
3. Stephen C. Meyer, Marcus Ross, Paul Nelson, and Paul Chien (2003), The Cambrian Explosion: Biology's Big Bang p.367 (see http://www.discovery.org/scripts/viewDB/filesDB-download.php?command=download&id=639)
4. Robert Deyes (2008), The Evolution Of An Alternative Theory: The Scientific Underpinnings of Intelligent Design, See
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