Evolved pollution tolerance in Gulf killifish (Fundulus grandis) from the Corpus Christi Inner Harbor, Texas, USA

The Corpus Christi Inner Harbor in Texas is a major center of industrial activity and contains high levels of persistent pollutants, including dioxins, furans, polycyclic aromatic hydrocarbons (PAHs), and polychlorinated biphenyls (PCBs). The Gulf killifish, Fundulus grandis, is an estuarine species inhabiting the Gulf of Mexico. F. grandis populations from the Houston Ship Channel (Galveston Bay, Texas) have been previously shown to be resistant to PCB-induced cardiac teratogenesis via a recalcitrant aryl hydrocarbon receptor (AHR) pathway. In this study, embryos from two F. grandis populations collected from the Corpus Christi Inner Harbor were exposed to varying doses of PCB-126 and evaluated for heart deformities at 144 h post fertilization. Both populations displayed significant resistance to PCB-induced cardiac teratogenesis compared to a reference population, representing the second documented cluster of adapted populations of F. grandis. Additionally, these populations exhibited lower basal cytochrome P4501A (CYP1A) activity (as measured via EROD assay) and reduced inducibility, indicating that a recalcitrant AHR pathway is at least partially responsible for the observed PCB resistance. Finally, we found that PCB-induced cardiac teratogenesis and CYP1A induction were highly correlated at the population level; however, individual CYP1A activity did not predict cardiac deformity. We propose a theoretical model in which inter-individual variation in CYP1A response explains this discrepancy and offers a conceptual framework for understanding individual variation within adapted populations. Collectively, these findings provide new insight into the mechanisms underlying adaptive responses to persistent pollutants and further establish F. grandis as a valuable model for evolutionary toxicology.