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Genetic basis for evolved tolerance to dioxin-like pollutants in wild Atlantic killifish: more than the aryl hydrocarbon receptor
Citation:
Nacci, D., D. Champlin, J. Martinson, E. Waits, D. Proestou, S. Karchner, M. Hahn, AND B. Clark. Genetic basis for evolved tolerance to dioxin-like pollutants in wild Atlantic killifish: more than the aryl hydrocarbon receptor. Society of Environmental Toxicology and Chemistry North America (SETAC NA) 36th Annual Meeting, Salt Lake City, UT, November 01 - 05, 2015.
Impact/Purpose:
This presentation describes experimental studies that contribute to our understanding of the ecological 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 (Fundulus heteroclitus) resident to some US urban and industrialized estuaries demonstrate recently evolved and extreme tolerance to toxic dioxin-like compounds (DLCs). Here we provide an unusually comprehensive accounting (69%) through Quantitative Trait Locus (QTL) analysis of the genetic basis for DLC tolerance in killifish resident to a PCB-contaminated Superfund site. Consistent with mechanistic knowledge of DLC toxicity in fish and other vertebrates, the aryl hydrocarbon receptor (ahr2) region accounts for 17% of trait variation; however, QTLs on an independent linkage group and their interactions have even greater explanatory power (44%). One QTL was also enriched in geographically disparate DLC-tolerant killifish populations, suggesting convergence in this independently evolving intra-specific trait. Research now focuses on genetic variation in one candidate gene nearby to this QTL, and its potentially causal role in DLC-tolerance. Together, results interpreted by leveraging Fundulus genomic resources and shared synteny among fish species suggest adaptation via inter-acting components of a complex stress response network, and provide new insight into genetic mechanisms of rapid evolution in the wild.