An Incompatibility between a Mitochondrial tRNA and Its Nuclear-Encoded tRNA Synthetase Compromises Development and Fitness in Drosophila

• DOI: 10.1371/journal.pgen.1003238
• Publication Date: 2013-01-31T21:34:28Z
• Authors: Colin D. Meiklejohn; Marissa A. Holmbeck; Mohammad A. Siddiq; Dawn N. Abt; David M. Rand; Kristi L. Montooth
• Keywords: Nuclear gene

Mitochondrial transcription, translation, and respiration require interactions between genes encoded in two distinct genomes, generating the potential for mutations nuclear mitochondrial genomes to interact epistatically cause incompatibilities that decrease fitness. Mitochondrial-nuclear epistasis fitness has been documented within populations species of diverse taxa, but rarely genetic or mechanistic basis these mitochondrial–nuclear elucidated, limiting our understanding which harbor variants causing disruption pathways processes are impacted by coevolution. Here we identify an amino acid polymorphism Drosophila melanogaster nuclear-encoded tyrosyl–tRNA synthetase interacts with a D. simulans mitochondrial-encoded tRNATyr significantly delay development, compromise bristle formation, fecundity. The incompatible genotype specifically decreases activities oxidative phosphorylation complexes I, III, IV contain subunits. Combined identity interacting alleles, this pattern indicates protein translation is affected interaction. Our findings suggest tRNAs their tRNA synthetases may be targets compensatory molecular evolution. Human diseases often genetically complex variable penetrance, interaction document provides plausible mechanism explain complexity.