A foundational question in evolutionary biology is the origin and maintenance of distinct species. New species form when a progenitor species is first partitioned such that gene flow between the two subgroups is limited. These subgroups accumulate distinct genetic differences over time both in response to their environement and as a consequenc of genetic drift that build up morphological or behavioral barriers between these groups. These barriers lead to reproductive isolation, the final step in the speciation process.

My research interests focus on exploring the genetic, behavioral, and environmental factors that contribute to speciation by integrating population genetic theory and computer simulations that model historic processes with large-scale datasets containing whole-genome and -transcriptome information for populations of interest.

Current Work

Eukaryotic genomes are partitioned between the nucleus, which stores autosomes and sex chromosomes, and certain organelles, like the mitochondria. These distinct genetic elements are differentially transmitted. Unlike autosomes that spend equal amounts of time in males and females, sex chromosomes spend either ⅔ of their time in the homogametic sex (i.e X or Z chromosome) or all of their time in the heterogametic sex (i.e Y or W chromosome). The mitochondrial genome, while present in both sexes, is exclusively maternally inherited. This transmission asymmetry can lead to genetic conflict, but we still lack a clear understanding of the sexually antagonistic interactions between these genes. 

I have developed analytical models and computer simulations to examine how transmission asymmetries of autosomal, sex chromosome-linked, and mitochondrial genes may both cause and resolve sexual conflicts. We confirmed earlier results showing that sexually antagonistic mitochondrial variants (female advantageous, male disadvantageous) can invade populations and further demonstrated that, while nearly all nuclear variants that mitigate this effect slowly spread throughout a population, Y chromosomal variants spread substantially faster.

We have experimentally explored mitochondrial-Y interactions by otherwise isogenic Drosophila melanogaster strains, differing only in the geographical origin of their mitochondrial genome and Y chromosome. We evaluated gene expression patterns across these lines to assay phenotypic differences, and we found that genes involved in male fertility, metabolism, and immunity showed differential expression between these lines not only confirming theoretical expectations that mitochondrial and Y chromosomal genes interact but also showing that these interactions influence phenotypes that are crucial for organismal survival.