Mechanistic Basis of Resistance to PCBs in Atlantic Tomcod from the Hudson River

Department of Environmental Medicine, New York University School of Medicine,Tuxedo, NY 10987, USA.
Science (Impact Factor: 33.61). 02/2011; 331(6022):1322-5. DOI: 10.1126/science.1197296
Source: PubMed


The mechanistic basis of resistance of vertebrate populations to contaminants, including Atlantic tomcod from the Hudson River
(HR) to polychlorinated biphenyls (PCBs), is unknown. HR tomcod exhibited variants in the aryl hydrocarbon receptor 2 (AHR2)
that were nearly absent elsewhere. In ligand-binding assays, AHR2-1 protein (common in the HR) was impaired as compared to
widespread AHR2-2 in binding TCDD (2,3,7,8-tetrachlorodibenzo-p-dioxin) and in driving expression in reporter gene assays in AHR-deficient cells treated with TCDD or PCB126. We identified
a six-base deletion in AHR2 as the basis of resistance and suggest that the HR population has undergone rapid evolution, probably
due to contaminant exposure. This mechanistic basis of resistance in a vertebrate population provides evidence of evolutionary
change due to selective pressure at a single locus.

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Available from: Nirmal K Roy, Mar 06, 2014
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    • "Such mechanisms (i.e. altered receptor/accessory protein interactions) would be in accordance with that described for DL PCB specific tolerance in the PCB resistant tomcod (Microgadus tomcod) found in the Hudson River (Wirgin et al., 2011). Notably, AhR variants found in sensitive versus tolerant "
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    • "It has been suggested as a model fish for ecotoxicological studies in South America (Mattos et al., 2010; Ferreira et al., 2012; Zimmer et al., 2012; Dorrington et al., 2012; Machado et al., 2013). The use of fish in toxicological studies includes the fate of contaminants in aquatic environments (Burnett et al., 2007; Matson et al., 2008) and genetic aspects involved in adaptation to survive under extreme polluted conditions (Williams and Oleksiak, 2008; Wirgin et al., 2011). Data from these studies help to elucidate the biochemical and molecular mechanisms involved in toxicity (Hahn et al., 2004). "
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