Statement of Research Interests and Experience
Populations of nearly all species exhibit at least some degree of differentiation among geographic locales. A continuing challenge is to describe population genetic architectures within species and to identify, and order, the evolutionary forces responsible for the observed subdivision. Broadly speaking, these forces involve migration or gene flow, random genetic drift, natural selection, mutational divergence, and the opportunity for genetic recombination mediated by the mating system. Finer considerations require a partitioning of these general categories into biological factors relevant for each group of organisms. My research combines theory, cell biology, comparative genomics and experimental evolution to examine intraspecific variation in Drosophila simulans.
Studies of sequence variation within members of the D. melanogaster subgroup have shown the explanatory power of the Drosophila model system and of the molecular evolutionary approach. At a population genetic level there is little subdivision within specific autosomal loci of these species (with the possible exception of D. melanogaster from Zimbabwe). There is, however, considerable geographic subdivision within the three mitochondrial haplotypes of D. simulans (siI, -II, and -III). Ballard (2000c) estimated the divergence time of the haplotypes is likely to be around 1.75 Myr. Despite this age, few mutations have accumulated within any of the mitochondrial DNA (mtDNA) lineages. This incongruity of high divergence among haplotypes and low diversity within each of them remains unexplained. My research addresses this conundrum.
The mitochondrial genome is a single linked molecule in Drosophila and the observed population subdivision may be caused by selective forces either intrinsic or extrinsic to the host genome. Intrinsic selective forces include both mitochondrial and nucleomitochondrial effects that may vary spatially. Extrinsic selective forces include any maternally inherited factor. One such factor is the alpha proteobacteria Wolbachia pipientis.
Future Research
My research program aims to develop a fuller appreciation of the selective forces responsible for shaping the variation of mitochondrial and nuclear DNA in D. simulans and the distribution of Wolbachia sequence variants that this species harbors. It is possible to independently study the evolution of mtDNA, nuclear DNA and Wolbachia. Indeed, rigorous case studies of each mtDNA haplotype, of specific nuclear genes, and of each Wolbachia sequence variant in D. simulans provide the basis for my current research. I now aim to take the next step by conducting parallel experimental studies to investigate mitochondrial and nucleomitochondrial interactions, and host-symbiont interactions. These studies involve developing theory, laboratory experimentation and field work. Theory development will be done in collaboration with Dr Michael Turelli. Laboratory experimentation will involve permuting the relationship between the mitochondrial and nuclear genomes and between the host and symbiont. Tim Karr is a collaborator on some of the laboratory experiments. Field work will ensure that the parameter estimates obtained for robust modeling of the maintenance and spatial spread of mitochondrial haplotypes and Wolbachia variants are as accurate as possible.