Research Interests
My lab studies evolutionary genetics using the model genetic organism Drosophila. We use classical, molecular and population genetics methods as well as functional and comparative genomics to study divergence between species and disrupted gene interactions in species hybrids. We are currently studying the genetic basis of speciation, regulatory evolution, and co-evolution between nuclear and mitochondrial genomes.
X chromosome regulation during spermatogenesis and speciation
In many taxa, including Drosophila, hybrid male sterility evolves earlier following speciation than hybrid female sterility or hybrid inviability, and the density of factors causing hybrid male sterility is many times higher on the X chromosome than on the autosomes. The reasons for these patterns are not understood. We are studying the genetic control of X-chromosome and autosomal gene expression during spermatogenesis in D. melanogaster, and identifying the genes responsible for sterility in hybrid males between D. simulans and D. mauritiana.
Genetic dissection of regulatory evolution
Gene expression evolves by changes both to trans-regulatory factors and cis-regulatory sequences. We are studying the genetic basis for differences in genome-wide gene expression between D. simulans and D. mauritiana. We seek to understand the evolutionary and molecular basis for differences between cis-regulatory and trans-regulatory divergence in patterns of dominance, the degree of sexual dimorphism, the likelihood of causing regulatory incompatibilities, and the contribution of these two modes of gene regulation to functional divergence between species.
Co-evolution of mitochondrial and nuclear genomes
In most eukaryotes, nuclear and mitochondrial genomes co-evolve in order to maintain proper metabolic function. We study the effects of mtDNA and nuclear genome evolution in diverging lineages and the causal substitutions that disrupt mitochondrial function in species hybrids. We are also interested in how mito-nuclear interactions can lead to the variable penetrance and complex genetic basis for many human mitochondrial diseases.