Transcriptomic assessment of resistance to effects of an aryl hydrocarbon receptor (AHR) agonist in embryos of Atlantic killifish (Fundulus heteroclitus) from a marine Superfund site

dc.contributor.author Oleksiak, Marjorie F.
dc.contributor.author Karchner, Sibel I.
dc.contributor.author Jenny, Matthew J.
dc.contributor.author Franks, Diana G.
dc.contributor.author Mark Welch, David B.
dc.contributor.author Hahn, Mark E.
dc.date.accessioned 2011-07-11T20:01:17Z
dc.date.available 2011-07-11T20:01:17Z
dc.date.issued 2011-05-24
dc.description © The Author(s), 2011. This article is distributed under the terms of the Creative Commons Attribution License. The definitive version was published in BMC Genomics 12 (2011): 263, doi:10.1186/1471-2164-12-263. en_US
dc.description.abstract Populations of Atlantic killifish (Fundulus heteroclitus) have evolved resistance to the embryotoxic effects of polychlorinated biphenyls (PCBs) and other halogenated and nonhalogenated aromatic hydrocarbons that act through an aryl hydrocarbon receptor (AHR)-dependent signaling pathway. The resistance is accompanied by reduced sensitivity to induction of cytochrome P450 1A (CYP1A), a widely used biomarker of aromatic hydrocarbon exposure and effect, but whether the reduced sensitivity is specific to CYP1A or reflects a genome-wide reduction in responsiveness to all AHR-mediated changes in gene expression is unknown. We compared gene expression profiles and the response to 3,3',4,4',5-pentachlorobiphenyl (PCB-126) exposure in embryos (5 and 10 dpf) and larvae (15 dpf) from F. heteroclitus populations inhabiting the New Bedford Harbor, Massachusetts (NBH) Superfund site (PCB-resistant) and a reference site, Scorton Creek, Massachusetts (SC; PCB-sensitive). Analysis using a 7,000-gene cDNA array revealed striking differences in responsiveness to PCB-126 between the populations; the differences occur at all three stages examined. There was a sizeable set of PCB-responsive genes in the sensitive SC population, a much smaller set of PCB-responsive genes in NBH fish, and few similarities in PCB-responsive genes between the two populations. Most of the array results were confirmed, and additional PCB-regulated genes identified, by RNA-Seq (deep pyrosequencing). The results suggest that NBH fish possess a gene regulatory defect that is not specific to one target gene such as CYP1A but rather lies in a regulatory pathway that controls the transcriptional response of multiple genes to PCB exposure. The results are consistent with genome-wide disruption of AHR-dependent signaling in NBH fish. en_US
dc.description.sponsorship This work was supported in part by National Institutes of Health grants P42ES007381 (Superfund Basic Research Program at Boston University) and by a grant from the WHOI Ocean Life Institute. en_US
dc.format.mimetype application/pdf
dc.identifier.citation BMC Genomics 12 (2011): 263 en_US
dc.identifier.doi 10.1186/1471-2164-12-263
dc.identifier.uri https://hdl.handle.net/1912/4662
dc.language.iso en en_US
dc.publisher BioMed Central en_US
dc.relation.uri https://doi.org/10.1186/1471-2164-12-263
dc.rights Attribution 2.0 Generic *
dc.rights.uri http://creativecommons.org/licenses/by/2.0 *
dc.title Transcriptomic assessment of resistance to effects of an aryl hydrocarbon receptor (AHR) agonist in embryos of Atlantic killifish (Fundulus heteroclitus) from a marine Superfund site en_US
dc.type Article en_US
dspace.entity.type Publication
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Figure S1. Loop design for microarray hybridizations
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Additional file 3: Figure S2. Volcano plots illustrating gene expression differences at 5, 10, and 15 dpf.
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Additional file 2: Table S1. Significant differently expressed genes: Results from 2-way ANOVA.
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Additional file 4: Table S2. Differential gene expression and PCB inducibility in pairwise comparisons of NBH and SC embryos at 5, 10, and 15 dpf.
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