Meeting Abstract
Hydrogen sulfide (H2S) is a natural toxicant that creates extreme environmental conditions in some aquatic environments. Its toxic effects primarily result from the inhibition of the mitochondrial respiratory chain and the suppression of aerobic ATP production. Some metazoans have adapted to H2S-rich environments through increased H2S detoxification ability, structural changes of toxicity targets in the respiratory chain, and symbioses with microbes. However, H2S interacts with a variety of biological molecules, and it remains largely unexplored whether adaption also involves modification of alternative molecular targets. For example, H2S binds to the oxygen transport proteins myoglobin and hemoglobin, which renders them nonfunctional. This is particularly relevant because sulfidic environments are also hypoxic. We investigated twelve evolutionary independent lineages of fish (family Poeciliidae) that have colonized sulfide springs throughout the Americas, including the genera Gambusia, Limia, Poecilia, Pseudoxiphophorus, and Xiphophorus. Using RNA-sequencing data, we compared the expression of hemoglobin and myoglobin genes between sulfide spring populations and closely related populations in adjacent non-sulfidic environments. In addition, we tested for positive selection on oxygen transport genes in sulfide spring lineages. Our results show upregulation of genes encoding for oxygen transport proteins. In addition, some lineages of sulfide spring fishes exhibit elevated rates of non-synonymous amino acid substitutions, suggesting that oxygen transport genes are under selection. In combination with previous research, our study suggests that adaptation to H2S-rich environments involves modification of multiple physiological pathways.
