Solving an evolutionary puzzle: Atlantic killifish thriving in highly polluted water

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For four decades, waste from nearby manufacturing plants flowed into the waters of New Bedford Harbor — an 18,000-acre estuary and busy seaport. The harbor, which is contaminated with polychlorinated biphenyls (PCBs) and heavy metals, is one of the EPA’s largest Superfund cleanup sites.It’s also the site of an evolutionary puzzle that researchers at Woods Hole Oceanographic Institution (WHOI) and their colleagues have been working to solve.Atlantic killifish — common estuarine fishes about three inches long — are not only tolerating the toxic conditions in the harbor, they seem to be thriving there. How have they been able to adapt and live in such a highly contaminated environment?In a new paper published in BMC Evolutionary Biology, researchers found that changes in a receptor protein, called the aryl hydrocarbon receptor 2 (AHR2), may explain how killifish in New Bedford Harbor evolved genetic resistance to PCBs.Killifish are prey fish that do not migrate. They live their whole lives in the same area, generally within a few hundred yards of the spot where they were hatched. Unlike fish that may come in and out of the harbor sporadically during the summer months to feed, the killifish are there year round and spend winters burrowing into the contaminated sediment.Normally when fish are exposed to harmful chemicals, the body steps up production of enzymes that break down the pollutants, a process controlled by the AHR2 protein. Some of the PCBs are not broken down in this way, and their continued stimulation of AHR2 disrupts cellular functions, leading to toxicity. In the New Bedford Harbor killifish, the AHR2 system has become resistant to this effect.”The killifish have managed to shut down the pathway,” said Mark Hahn, a biologist at WHOI and coauthor of the paper. “It’s an example of how some populations are able to adapt to changes in their environment — a snapshot of evolution at work.”The research team, which includes colleagues from the Atlantic Ecology Division of the U.S. Environmental Protection Agency, the Boston University School of Public Health, and the University of North Carolina at Charlotte, used a “candidate gene” approach, sequencing the protein-coding portion of three candidate resistance genes (AHR1, AHR2, AHRR) in fish from the New Bedford site and six other locations, both clean and polluted, along the northeast coast.Looking for single nucleotide polymorphisms (SNPs) or subtle variations in the DNA sequence, they found differences in AHR2, which plays an important role in mediating toxicity in early life stages.”The function of this receptor is what mediates the toxic effects,” said Sibel Karchner, a coauthor and biologist in Hahn’s lab. “If you don’t have a functional receptor, then you’re not going to get the toxic effects as much as a fish that does.”AHR2 in killifish has 951 amino acids and nine of those vary among individuals. …


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