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Genetic Architecture of Pollution Resistance in Multiple Populations of Killifish
Citation:
Miller, J., B. Clark, D. Champlin, D. Nacci, AND A. Whitehead. Genetic Architecture of Pollution Resistance in Multiple Populations of Killifish. Society of Environmental Toxicology and Chemistry North America (SETAC-NA) 39th Annual Meeting, Sacramento, California, November 04 - 08, 2018.
Impact/Purpose:
Population differences in sensitivity can affect how we interpret contaminant exposure and effect. Sometimes population differences arise because of adaptation to chronic exposure to contaminants, and studying these adapted populations helps us understand how organisms vary in sensitivity to chemicals. It is important to understand how variation in specific genes or groups of genes affects organism response to contaminants, so that we can better predict sensitivity to contaminants across many different populations and species. In this study, we cross-bred Atlantic killifish from populations living in estuarine Superfund sites polluted with dioxin-like chemicals and/or polycyclic aromatic hydrocarbons with fish from reference sites. We then exposed their descendants to contaminants in the laboratory, assessed the impact on their embryonic development, and individually sequenced their genomes. This information was used to identify regions of the genome associated with high or low response to the contaminant. This work identifies genes that are important in controlling sensitivity to dioxin-like contaminants and will help to build better predictions of population response to these contaminants.
Description:
Multiple populations of Atlantic Killifish (Fundulus heteroclitus) that reside in heavily polluted habitats along the Atlantic coast of North America have repeatedly and rapidly evolved resistance to highly toxic dioxin-like pollutants (DLCs), which act through the aryl hydrocarbon receptor (AHR) signaling pathway. Prior studies using Quantitative Trait Locus (QTL) mapping identified some of the genetic markers associated with DLC resistance in a single resistant killifish population, and multi-population genome-wide scans also showed that wild DLC-resistant killifish populations have some shared and some unique genomic regions under selection, including some associated with DLC resistance. These studies and others suggest that resistance to the toxic effects of DLCs, such as cardiovascular and other developmental deformities, is extreme but not identical in resistant killifish populations. Here, we extended the QTL approach to four resistant killifish populations distributed from Massachusetts to Virginia, and employed high-density QTL interval mapping to compare and contrast genetic regions associated with DLC resistance in these diverse populations. Our results show that in all four populations a common genomic region associates with DLC resistance, which includes two AHR pathway genes (AHR1b/2b) that did not show obvious signatures of selection in population genome scan data. Another AHR pathway gene (the aryl hydrocarbon receptor interacting protein, AIP) is in a genomic region showing strong signatures of selection and is associated with resistance in three of the four populations. These results also suggest that variation in AHR1b/2b may have evolved by soft sweeps on standing genetic variation in resistant populations, which are difficult to detect by traditional selection scan methods. These results suggest that AIP is an important gene in the evolutionary response to complex, heavily contaminated environments. Our findings, integrated with population genomic scans for selection, reveal the unique evolutionary trajectories that led to evolved DLC resistance in wild killifish. QAPP AED-PEB-DN-2016-01-00