A genetic mutation allows Hudson river fish to adapt to PCBs

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A research group led by an NYU School of Medicine scientist discovered a genetic variant that allows a fish in the Hudson River to live in waters heavily polluted by PCBs. In a study published in the February 18, 2011, online issue of Science, they report that a population of Hudson River fish apparently evolved rapidly in response to the toxic chemicals, which were first introduced in 1929, and were banned fifty years later. PCBs, or polychlorinated biphenyls, were used in hundreds of industrial and commercial applications, especially as electrical insulators.

'We've found evolutionary change going on very quickly due to toxic exposure, and just one gene is responsible for it,' says Isaac Wirgin, a population geneticist, associate professor of environmental medicine at NYU School of Medicine, and the study's lead investigator. 'There are not many examples of this in the scientific literature.'

General Electric released approximately 1.3 million pounds of PCBs into the Hudson River from 1947 to 1976. The Atlantic tomcod, Microgadus tomcod, is a common bottom-feeding fish in the Hudson that is not usually eaten by humans. The fish, which typically reaches a length of 10 inches, had long been known to survive exposure to PCBs, and levels of the chemical in its liver are among the highest reported in nature. However, scientists did not understand the biological mechanism that allowed the tomcod to survive chemical exposures that kill most other fishes.

Dr. Wirgin and scientists at NOAA Fisheries Service in New Jersey and the Woods Hole Oceanographic Institution in Massachusetts spent four years capturing tomcod from contaminated and relatively clean areas of the Hudson River during the winter months, when tomcod spawn in the river. The fish were screened for genetic variants in a gene encoding a protein known to regulate the toxic effects of PCBs, which is called the aryl hydrocarbon receptor2, or AHR2. This gene also is involved in mediating the effects of other halogenated hydrocarbon compounds, a group that includes PCBs.

Slight alterations—the deletion of only six base pairs in DNA of the AHR2 gene—appear to protect tomcod from PCBs, according to the study. Normally, when unaltered AHR2 binds to PCBs, it triggers a cascade of reactions that transmit the toxic effects of the compound. However, the study found that PCBs bind poorly to the variant AHRs, which apparently blunts the chemicals' effects.

Tomcod from cleaner waters occasionally carried mutant AHR2, suggesting that these variants existed in minor proportions prior to PCB pollution, says Dr. Wirgin. After the chemical was released, tomcod carrying the mutation had an advantage over others in the population because PCBs otherwise lead to lethal heart defects in young fish. The study's findings suggest that this advantage drove genetic changes in these fish over some fifty years. 'We think of evolution as something that happens over thousands of generations,' says Dr. Wirgin. 'But here it happened remarkably quickly.'

The study co-authors are: Nirmal K. Roy and Matthew Loftus, the NYU School of Medicine; R. Christopher Chambers, the NOAA Fisheries Service, Highland, New Jersey; and Diana G. Franks and Mark E. Hahn, Woods Hole Oceanographic Institution.

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