Meeting Abstract
Incompatibility between gene products encoded by mitochondrial and nuclear genomes (mitonuclear incompatibilities) is a mechanism of hybrid incompatibility hypothesized to serve as a major contributor to speciation. Oxidative phosphorylation (OXPHOS) consists of genes encoded by both genomes and is responsible for the fundamental process of aerobic ATP production. OXPHOS is a candidate for mitonuclear incompatibilities as hybridization between divergent populations or species can lead to the breakup of co-adapted mitonuclear gene products. Hydrogen sulfide (H2S) rich habitats provide an ideal natural setting for testing hypotheses about mitonuclear incompatibility, as H2S is extremely toxic to most organisms due to its inhibition of OXPHOS. H2S toxicity results in direct selection on OXPHOS in habitats with high concentrations of H2S. Despite strong selection, tolerance to high concentrations of environmental H2S is known from multiple evolutionarily independent populations of fish in the family Poeciliidae. Direct selection on OXPHOS in sulfidic populations could lead to the coevolution of mitonuclear interacting proteins that do not function when combined with subunits originating from non-sulfidic populations, resulting in hybrid incompatibilities and contributing to ecological speciation. Using transcriptome data and protein structure modeling, we investigated signatures of positive selection and mitonuclear coevolution in the OXPHOS pathways of sulfidic populations. Analyses of molecular evolution consistently indicate relaxed selection on OXPHOS genes in sulfidic populations. Furthermore, some lineages of sulfide spring poeciliids show signatures of strong positive selection on OXPHOS genes as well as coevolution between mitochondrial and nuclear OXPHOS genes.
