Meeting Abstract
Phenotypes do not emerge solely as a result of variation at a single locus, but can be altered by genetic variation at other loci (epistasis), environmental variation (plasticity), and epigenetic modifications. Complicating matters further, most studies only consider the nuclear genome when examining genotype-to-phenotype relationships. However, emerging evidence suggests mitonuclear epistasis is rampant – different phenotypes arise when the same nuclear genome is placed against different mitochondrial genotypes. The environment can further modify mitonuclear epistasis (G x G x E interactions). “Phenotype” can also be defined across biological scales, from the expression of genes to whole-organism fitness. In this talk I will discuss a series of studies linking mitochondrial genotype to mitochondrial and whole-organism phenotypes. First, we ask whether extreme variation seen in mitochondrial genomes of the angiosperm genus Silene affects mitochondrial function, despite having little noticeable effects at the organismal level. Next, we explore whether placing different mitochondrial genotypes against a common nuclear genome affects mitochondrial function and organismal phenotypes in Silene. Finally, we present a meta-analysis of mitochondrial and whole-animal oxygen consumption in response to temperature to ask how similarly phenotypes at different scales vary in response to environment. Taken together, our results suggest that phenotypic variation should be explored in response to genetic variation at both mito- and nuclear loci, across environments, and across biological scales.
