| Summary: | The Deepwater Horizon (DWH) oil spill released approximately 780,000 m3 of oil into the Gulf of Mexico in 2010, exposing pelagic and coastal marine ecosystems to oil and its main toxic components, polycyclic aromatic hydrocarbons (PAHs). Previous studies in aquatic and terrestrial organisms following the oil spill have shown an increase in the expression of the cytochrome P4501A (cyp1 a) gene, a biomarker of PAHs exposure. In studies of Pacific herring and pink salmon, exposure to crude oil decreased cardiorespiratory performance in critical swimming speed tests and caused morphological changes in ventricular length and outflow tracts. However, terrestrial organisms differ from aquatic organisms in their mechanisms for PAHs exposure, and little is known about the effects of oil exposure in these species. Transcriptomic analyses of a terrestrial organism, the seaside sparrow (Ammospiza maritima), have shown differential gene expression between exposed and unexposed organisms. This experiment will build on those early results by investigating the cardiotoxicity of PAHs exposure in the seaside sparrow by conducting real-time PCR and measuring the expression of the jun gene in exposed and control birds. The jun gene is a proto-oncogene linked with cardiac enlargement and congenital heart anomalies. We hypothesis that the jun gene will have increased expression in exposed organisms relative to the control group. This experiment will investigate whether cardiotoxicity due to oil exposure is a universal effect in common between terrestrial and aquatic organisms, with implications for using this gene as a biomarker of toxicity in future studies.
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