Meeting Abstract

89-4  Sunday, Jan. 6 11:00 - 11:15  Genetic, biochemical, and physiological adaptation in fish inhabiting sulfide-rich environments BARTS, N*; HENPITA, C; GREENWAY, R; ARNDT, S; SHAW, J; TOBLER, M; Kansas State University; Oklahoma State University; Kansas State University; University of Cambridge; Oklahoma State University ; Kansas State University

A fundamental goal of evolutionary biology is to understand the relationship between genotype and phenotype, providing insights into physiological, biochemical, and genetic mechanisms underlying adaptation. Exploring how changes across levels of biological organization ultimately lead to phenotypes observed in nature benefits from studying organisms that experience environmental conditions with predictable consequences on physiological function. Hydrogen sulfide (H2S) is a natural toxicant that inhibits aerobic ATP production by binding to cytochrome c oxidase (COX) in the mitochondrial respiratory chain and is regulated by the sulfide:quinone oxidoreductase (SQR) pathway. We used multiple population pairs of Poecilia mexicana in habiting sulfidic and non-sulfidic habitats to show that genes encoding toxicity targets and detoxification pathways are under positive selection and differentially expressed. In addition, we explored the influence of hydrogen sulfide on enzymatic function of COX, other mitochondrial respiratory complexes, and SQR, and how changes in the functionality of these enzymes influence mitochondrial physiology. Specifically, we quantified variation in enzymatic activity in the mitochondrial complexes and key detoxification genes and relate changes in enzymatic function to mitochondrial performance in the presence and absence of H2S. Preliminary results provide evidence for selection on Complex I and IV in sulfide-tolerant populations of P. mexicana, that concentrations of H2S within mitochondria increase more quickly in sulfide-intolerant populations exposed to H2S, and that mitochondrial performance deteriorates more quickly in sulfide-intolerant populations exposed to H2S.