The severity of a mitochondrial-nuclear incompatibility depends upon the developmental thermal environment. Kristi L. Montooth, Luke A. Hoekstra, Mohammad A. Siddiq. Dept Biol, Indiana Univ, Bloomington, IN.

   Energetic performance can create a dynamic context for the effects of mutations. Given that protein-protein and RNA-protein interactions between mitochondrial and nuclear genomes underlie energetic performance in eukaryotes, we expect that the effects of many mitochondrial mutations will be conditional on variation in the nuclear genome. Furthermore, in ectotherms, the phenotypic effects of these mitochondrial-nuclear interactions may be conditional on the thermal environment, because temperature impacts rates of biological processes and can place high demand on energy use. I will present data that demonstrate strong thermal-dependence of the phenotypic effects of a mitochondrial-nuclear genetic interaction. We have previously found that a mitochondrial-nuclear incompatibility between a single nucleotide polymorphism in the D. simulans mt-tRNA-Tyr and a non-synonymous polymorphism in the nuclear-encoded D. melanogaster mt-Tyr-tRNA synthetase encoded by Aatm severely affects development and reproduction via compromised mitochondrial protein translation (C.D. Meiklejohn, M.A. Holmbeck, M.A. Siddiq, D.N. Abt, D.M. Rand and K.L. Montooth manuscript in review). Remarkably, a shift in developmental temperature from 25C to 16C masks these deleterious effects, while a shift to 28C results in male and female sterility. Mitochondrial-nuclear epistatic effects on development time, pupation height and reproduction - traits that are associated with energetic state - are all worse when temperature accelerates the rate of life. I will present these results in the context of what we have recently learned about the molecular evolution and population genomics of Drosophilid mitochondrial versus nuclear genes relative to humans, mammals and other invertebrates.