We are using the Atlantic killifish population-based model system to elucidate the interaction of genetic variation and environmental exposures in the etiology of congenital heart disease.
We are investigating the role of AIP and its sequence variants in controlling sensitivity to diverse chemicals that act through the AHR. This project includes complementary studies involving zebrafish in vivo and human cells in vitro.
We are investigating the evolutionary trajectory and genetic and structural mechanisms underlying the evolution of AHR ligand-specificity. We are using ancestral sequence reconstruction (ASR) to “resurrect” ancestral AHR proteins and then determine their ligand-binding properties.
The goal of this research is to to elucidate the mechanisms by which vertebrate embryos respond to oxidative stress during development. We use zebrafish as a model system.