The thermal environment modifies mitochondrial-nuclear effects on insect metabolic performance and plasticity


Meeting Abstract

11.5  Saturday, Jan. 4 11:15  The thermal environment modifies mitochondrial-nuclear effects on insect metabolic performance and plasticity MONTOOTH, KL*; HOEKSTRA, LA; SIDDIQ, MA; Indiana University, Bloomington; Indiana University, Bloomington; Indiana University, Bloomington montooth@indiana.edu

Given that 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. In ectotherms, the effects of these mitochondrial-nuclear interactions are likely to depend upon the thermal environment, because temperature accelerates rates of biological processes and can increase demands on ATP pools. We have found that a mitochondrial-nuclear incompatibility between single nucleotide polymorphisms in a mitochondrial tRNA and its nuclear-encoded tRNA synthetase severely affects fitness via compromised mitochondrial protein translation in Drosophila (Meiklejohn et al. 2013 PLoS Genetics 9:e1003238). Here I present data showing that the deleterious effects of this interaction on development time, pupation height and reproduction – traits that are associated with energetic state – are ameliorated when larvae develop at 16°C and exacerbated at warmer temperatures, leading to complete sterility at 28°C. The incompatible genotype has a normal metabolic rate at 16°C but a significantly elevated rate at 25°C, consistent with the hypothesis that inefficient metabolism extends development in this genotype at warmer temperatures. Furthermore, the incompatibility decreases metabolic plasticity of larvae developed at 16°C, indicating that cooler temperatures do not completely mitigate the deleterious effects of this interaction. The expression of genetic interactions in some environments, but not others, weakens the efficacy of selection in removing deleterious epistatic variants from populations and may promote the accumulation of incompatibilities whose fitness effects will depend upon the environment in which hybrids occur.

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