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GENETIC ARCHITECTURE OF METABOLIC RATE: ENVIRONMENT SPECIFIC EPISTASIS BETWEEN MITOCHONDRIAL AND NUCLEAR GENES IN AN INSECT
Author(s) -
Arnqvist Göran,
Dowling Damian K.,
Eady Paul,
Gay Laurene,
Tregenza Tom,
Tuda Midori,
Hosken David J.
Publication year - 2010
Publication title -
evolution
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.84
H-Index - 199
eISSN - 1558-5646
pISSN - 0014-3820
DOI - 10.1111/j.1558-5646.2010.01135.x
Subject(s) - biology , mitochondrial dna , epistasis , nuclear gene , gene , genetics , nuclear dna , evolutionary biology , genetic variation , genetic architecture , genome , mitochondrion , evolutionary dynamics , phenotype , population , demography , sociology
The extent to which mitochondrial DNA (mtDNA) variation is involved in adaptive evolutionary change is currently being reevaluated. In particular, emerging evidence suggests that mtDNA genes coevolve with the nuclear genes with which they interact to form the energy producing enzyme complexes in the mitochondria. This suggests that intergenomic epistasis between mitochondrial and nuclear genes may affect whole‐organism metabolic phenotypes. Here, we use crossed combinations of mitochondrial and nuclear lineages of the seed beetle Callosobruchus maculatus and assay metabolic rate under two different temperature regimes. Metabolic rate was affected by an interaction between the mitochondrial and nuclear lineages and the temperature regime. Sequence data suggests that mitochondrial genetic variation has a role in determining the outcome of this interaction. Our genetic dissection of metabolic rate reveals a high level of complexity, encompassing genetic interactions over two genomes, and genotype × genotype × environment interactions. The evolutionary implications of these results are twofold. First, because metabolic rate is at the root of life histories, our results provide insights into the complexity of life‐history evolution in general, and thermal adaptation in particular. Second, our results suggest a mechanism that could contribute to the maintenance of nonneutral mtDNA polymorphism.