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The genomic landscape of rapid repeated evolutionary adaptation to toxic pollution in wild fish
Citation:
Reid, N., D. Proestou, B. Clark, W. Warren, J. Colbourne, J. Shaw, S. Karchner, M. Hahn, D. Nacci, M. Oleksiak, D. Crawford, AND A. Whitehead. The genomic landscape of rapid repeated evolutionary adaptation to toxic pollution in wild fish. SCIENCE. American Association for the Advancement of Science (AAAS), Washington, DC, 354(6317):1305-1308, (2016).
Impact/Purpose:
This manuscript describes genomic evaluations that contribute to our understanding of the ecological and evolutionary risks associated with chronic contaminant exposures to wildlife populations. Here, we assessed genetic patterns associated with long-term response to an important class of highly toxic environmental pollutants. Specifically, chemical-specific tolerance has rapidly and repeatedly evolved in an estuarine fish species resident to estuaries of the Atlantic U.S. coast. We used laboratory studies to characterize variation among laboratory-reared progeny of fish from populations known to vary in their sensitivity to these pollutants to infer mechanisms of toxicity and tolerance. Results of these studies demonstrate the value of molecular tools to diagnose and predict effects of chemical stressors and characterize the mechanisms and costs of toxic and compensatory responses to chemical stressors by wild populations. General impacts from this contribution include improved understanding by managers and scientists of links between human activities, natural dynamics, ecological stressors and ecosystem condition.
Description:
Atlantic killifish populations have rapidly adapted to normally lethal levels of pollution in four urban estuaries. Through analysis of 384 whole killifish genome sequences and comparative transcriptomics in four pairs of sensitive and tolerant populations, we identify the aryl hydrocarbon receptor–based signaling pathway as a shared target of selection. This suggests evolutionary constraint on adaptive solutions to complex toxicant mixtures at each site. However, distinct molecular variants apparently contribute to adaptive pathway modification among tolerant populations. Selection also targets other toxicity-mediatinggenes and genes of connected signaling pathways; this indicates complex tolerance phenotypes and potentially compensatory adaptations. Molecular changes are consistent with selection on standing genetic variation. In killifish, high nucleotide diversityhas likely been a crucial substrate for selective sweeps to propel rapid adaptation.
