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Does “Speedy Evolution” of PCB Resistance Help Darwinism?

Last week, the New York Times featured an article which reported that “in just 50 years, a fish has evolved a resistance to toxic chemicals polluting its Hudson River home, a new study finds.”

The NYT article reports,

Between 1947 and 1976, roughly 1.3 million pounds of polychlorinated biphenyls, or PCBs, were dumped in the Hudson by two General Electric facilities. The Atlantic tomcod, a small bottom-feeding fish, quickly accumulated high levels of the toxic compounds, which caused lethal heart defects in juveniles of the species.

Then, natural selection took over. In a matter of decades, a rare genetic mutation that allowed a small number of tomcod to tolerate PCB contamination spread through the broader population, allowing the species to thrive, scientists concluded after a four-year study.

The NYT article further notes that,

The tomcod had long been known for its remarkable tolerance to PCB pollution, but the biological mechanism responsible for its survival was unclear until now. Researchers found that a mutation to just one gene effectively blunted the chemical’s toxic effects, and that fish with the mutation survived and reproduced while those without it died off.

From a superficial reading of the NYT article, a casual reader may be tempted to think that what has been observed here is an instance of neo-functionalisation — that is to say, an advantageous instance of adaptive novelty. One might further be left with the impression that such an instance aptly documents the causal power and brilliance of the neo-Darwinian mechanism, or that this somehow demonstrates the causal sufficiency of chance and necessity to account for many of the highly complex and sophisticated adaptations we observe in living systems. After all, here it is: the Darwinian mechanism in action, right before our very eyes! Look at all the work a simple point mutation can do in facilitating resistance to otherwise toxic PCB. What have we ID proponents been thinking all these years?

But before the triumphal celebrations begin, wouldn’t it be wise to look at the original research, which appeared in the journal, Science, last week? While the NYT commentators may want the uninitiated reader to come away with the impression that this is an impressive feat which has been accomplished by the Darwinian mechanism, the original paper tells a very different story.

The paper [Isaac Wirgin, Nirmal K. Roy, et al. (2011). “Mechanistic Basis of Resistance to PCBs in Atlantic Tomcod from the Hudson River.” Science.] reports that,

The mechanistic basis of resistance of vertebrate populations to contaminants, including Atlantic tomcod from the Hudson River (HR) to polychlorinated biphenyls (PCBs), is unknown. HR tomcod exhibited variants in the aryl hydrocarbon receptor2 (AHR2) that were nearly absent elsewhere. In ligand binding assays, AHR2-1 protein (common in HR) was impaired compared to widespread AHR2-2 in binding TCDD (2,3,7,8-tetrachlorodibenzo-p-dioxin) and in driving expression in reporter gene assays in AHR-deficient cells treated with TCDD or PCB126. We identified a six-base deletion in AHR2 as the basis of resistance and suggest that the HR population has undergone rapid evolution probably due to contaminant exposure. The mechanistic basis of resistance in a vertebrate population provides evidence of evolutionary change due to selective pressure at a single locus. [Emphasis mine]

As it turns out, then, the mechanistic basis for fish resistance to PCB is a loss of function adaptive mutation at a single locus, resulting from a six-base deletion in a particular gene, AHR2. The receptor gene, AHR2, is ordinarily involved in mediating toxicity. In the study, the researchers find that the protein specified by the AHR2 gene is missing two of the 1,104 amino acids which are ordinarily found in the protein. This means that the receptor binds with weaker affinity to the PCB, conferring a measure of resistance to the fish. But such resistance does not come without a cost, as the associated genetic changes result in the tomcod becoming sensitive to other toxic compounds, and their ability to degrade such toxic compounds is reduced. The paper also discusses the mechanistic basis of resistance to other toxic compounds, such as polycyclic aromatic hydrocarbons (PAHs) and Tetrachlorodibenzo-p-dioxins (TCDD). The paper reports,

The mechanistic basis of variation in sensitivities to PAHs and TCDD between inbred mouse strains (10) and among avian species resulted from one or two amino acid substitutions at critical residues within the AHR LBD that reduce the binding affinities to ligand. We also observed substantially reduced binding affinity for TCDD in resistant tomcod, but this did not result from variation within the LBD.

This is all perfectly consistent with what would be predicted by an ID paradigm, and conforms neatly to the predictions which one would make in view of Michael Behe’s thesis outlined in The Edge of Evolution and, more recently, in the Quaterly Review of Biology. If this is among the best case scenarios with respect to what the Darwinian mechanism can do, then the paradigm is in trouble.

Jonathan McLatchie

Fellow, Center for Science and Culture
Dr. Jonathan McLatchie holds a Bachelor's degree in Forensic Biology from the University of Strathclyde, a Masters (M.Res) degree in Evolutionary Biology from the University of Glasgow, a second Master's degree in Medical and Molecular Bioscience from Newcastle University, and a PhD in Evolutionary Biology from Newcastle University. Currently, Jonathan is an assistant professor of biology at Sattler College in Boston, Massachusetts. Jonathan has been interviewed on podcasts and radio shows including "Unbelievable?" on Premier Christian Radio, and many others. Jonathan has spoken internationally in Europe, North America, South Africa and Asia promoting the evidence of design in nature.