Adaptation to poison, evolution at work

Adaptation to poison, evolution at work

Prior posts have noted the wide diversity of selection factors (well beyond Darwin's original thesis) that are able to influence evolution, or what individuals of a population will survive to procreate and define the nature of the future population.  Among factors cited in previous posts were toxicants and poisons; another example of such selection factors was published recently.

From 1947 to 1976, two General Electric manufacturing plants along the Hudson River produced PCB's.  As a result, the level of PCB's and dioxins in the liver of the Hudson's Atlantic tomcod population rose to be among the highest seen in nature.  Because these fish are not able to detoxify PCB's, the question arose -- how did they survive such an exposure.  Researchers have now found that the tomcod's protection derives from a single gene mutation.  In its unmutated form, the gene is responsible for producing a protein that defines PCB's toxicity.

All vertebrate cells contain molecules (aryl hydrocarbon receptors, or AHR's) that bind to dioxins and related compounds.  Once dioxins and related compounds diffuse into an exposed cell, each molecule can mate with a AHR and together they eventually pick up a third molecule.  This trio can then dock with select segments of DNA in the cell's nucleus to inappropriately turn on genes that can poison the host animal.

The tomcod has two types of AHR's, in this case known as AHR-2.  One naturally occurring AHR-2 variant takes five times more of the pollutants to get the requisite binding that is needed compared to the "conventional" AHR-2.  In local rivers relatively free of dioxins and PCB's, 95% of tomcod possess AHR-2 only in the conventional form; but, in the PCB-rich Hudson, the only kind of AHR-2 protein in 99 percent of tomcod is the poorly binding variant.  The mutant receptor appears to have evolved long ago and to be widely dispersed in the tomcod population.  But in the Hudson, fish with the gene to make the mutant receptor have thrived, while those without it have died out.  The result is that these tomcod survive and also store the PCB's and related compounds in their fat.  While this helps the fish, it provides a reservoir of the toxin that is passed up the food-chain.  Ultimately, those fish often consumed by humans have very large concentrations of PCB's and related compounds.

The study of tomcod can be found at  Another good discussion of the general issue can be found at