Meeting Abstract

S6-3  Saturday, Jan. 5 09:00 - 09:30  The role of mitonuclear incompatibilities during ecological speciation in extremophile poeciliid fishes GREENWAY, R.*; HAVIRD, J.C.; KELLEY, J.L.; TOBLER, M.; Kansas State University; University of Texas at Austin; Washington State University; Kansas State University

Hybrid breakdown due to mitonuclear incompatibilities (incompatibilities between genes encoded by the mitochondrial [mt] and nuclear [nuc] genomes) is hypothesized to serve as a major contributor to speciation. Oxidative phosphorylation (OXPHOS), an essential biological pathway consisting of mitonuclear protein complexes, is a candidate for mitonuclear incompatibilities as hybridization between lineages can lead to the breakup of co-adapted OXPHOS proteins. Hydrogen sulfide (H2S) rich habitats provide an ideal setting for testing hypotheses about mitonuclear incompatibility. H2S is extremely toxic to most organisms because it inhibits OXPHOS, resulting in direct selection on OXPHOS. Despite extreme toxicity, tolerance to environmental H2S is known from evolutionarily independent lineages of fish in the family Poeciliidae that have colonized H2S-rich freshwater springs. Strong selection on OXPHOS genes should lead to the evolution of tightly co-adapted mitonuclear gene complexes in sulfidic lineages, increasing the likelihood of mitonuclear incompatibilities upon hybridization with non-sulfidic lineages. Using sequence data from sulfidic and closely related non-sulfidic lineages, we found evidence for positive selection on mt OXPHOS genes in sulfidic lineages, as well as on corresponding nuc OXPHOS genes in a subset of lineages. Protein structure modeling revealed amino acid substitutions occur at contact residues between mt and nuc encoded proteins in some lineages. Structural models of OXPHOS complexes for these lineages were used to quantify the effect of these substitutions on the thermodynamic stability of “hybrids” created by recombining OXPHOS subunits from sulfidic and non-sulfidic lineages in silico.