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Genetic architecture of evolved tolerance to PCBs in the estuarine fish Fundulus heteroclitus
Citation:
WAITS, E. R., S. Morris, B. Rinner, D. PROESTOU, D. M. CHAMPLIN, AND D. E. NACCI. Genetic architecture of evolved tolerance to PCBs in the estuarine fish Fundulus heteroclitus. Presented at SETAC North America, Boston, MA, November 13 - 17, 2011.
Impact/Purpose:
This research aims to evaluate the utility of population genetic measurements for describing the current condition and vulnerabilities of biological populations exposed to anthropogenic stressors.
Description:
Populations of Atlantic killifish (F. heteroclitus) resident to coastal estuarine habitats contaminated with halogenated aromatic hydrocarbons (HAHs) exhibit heritable resistance to the early life-stage toxicity associated with these compounds. Beyond our knowledge of the aryl hydrocarbon receptor (AHR) and its role in mediating this toxicity, little else is known concerning the precise downstream targets responsible for this adaptation. In the present study, we performed a genome-wide survey for quantitative genetic variation among differentially sensitive killifish in order to elucidate the genetic basis of evolved tolerance. Following exposure to PCB126, the recombinant generation of a genetic cross between PCB-sensitive (Block Island, RI) and PCB-tolerant (New Bedford, MA) killifish were phenotyped to determine sensitivity and genotyped with a dense panel of co-dominant molecular markers distributed across the genome. Multiple loci were identified strongly associated with PCB tolerance--some acting alone and others via additive and epistatic interactions. Together, these loci account for at least 44% of the phenotypic variance observed in susceptibility following PCB126 exposure between Block Island and New Bedford killifish. These data demonstrate that PCB126-induced developmental toxicity is a complex trait influenced by gene x gene and gene x environment interactions, and provide insight to the evolutionary basis of evolved tolerance to chemical contaminants in wild populations.