evolutionary genetics, host-microbe interactions, speciation, and other stuff
We are a collaborative team of researchers studying Wolbachia spread and the evolution of reproductive isolation (usually not related!) in many host systems (usually Drosophila). Our current projects combine approaches from genomics, genetics, cell biology, and population biology to better understand Wolbachia effects on host physiology and fitness that underlie its spread. Our discoveries also inform efforts to spread Wolbachia from Drosophila through mosquito populations for biocontrol of human disease (particularly dengue and Zika). Field work takes us from local orchards to sites overseas where we sample Wolbachia-infected flies from several continents. We are fortunate to conduct our lab research at the University of Montana in beautiful Missoula, Montana.
Acquisition, spread, and maintenance of Wolbachia infections
By comparing mitochondrial, nuclear, and Wolbachia genomic variation, we are determining the modes by which hosts acquire their Wolbachia (i.e., from common ancestors versus through introgression or via horizontal transfer). We are also evaluating Wolbachia frequency variation through time and space in many host species. Several projects are focused on identifying Wolbachia effects on host physiology and fitness that enable Wolbachia to spread from low frequencies. In total, we are currently working on about 20 Wolbachia-infected Drosophila systems.
Genetic basis of Wolbachia phenotypes
Several projects are assessing the genetic basis of Wolbachia effects on host physiology and fitness that underlie Wolbachia spread. For example, we have demonstrated that factors in host genomes modify the strength of Wolbachia-induced cytoplasmic incompatibility (CI). (CI reduces the egg hatch of uninfected females mated with Wolbachia-infected males.) In multiple systems, we have found support for the theoretical prediction that selection does not act to maintain CI, with evidence that non-CI causing strains often have remnants of CI loci in their genomes. Very recent results have also revealed that transposable elements within WO prophage regions may mediate horizontal transfer of CI-associated loci between divergent Wolbachia . The figure below shows that wYak-clade Wolbachia prophage regions contain two sets of CI loci, with transposon-mediated horizontal movement of divergent Type 4 cin loci into wYak-clade Wolbachia genomes—these loci are absent from sister wMel, but present in distantly related wPip.
Wolbachia maternal transmission
Wolbachia infections are usually polymorphic due to imperfect maternal transmission. Non-CI-causing Wolbachia like wMel often persist at intermediate frequencies that fluctuate, potentially due to variable transmission rates. Our field and lab work is demonstrating that wMel-like Wolbachia titer and transmission depend on temperature. Using mathematical models—in combination with estimates of imperfect transmission, CI, and fitness effects—we are determining the causes of Wolbachia frequency variation in host populations.
Local adaptation and reproductive isolation
We are interested in understanding local adaptation within, and the evolution of reproductive isolation between, host species. In the past this research has involved assessing the cell basis of temperature adaptation in natural and experimentally evolved Drosophila populations. More recently, we've described a new D. yakuba-D. teissieri hybrid zone, in collaboration with Daniel Matute's group. Because Wolbachia are maternally transmitted endosymbionts, hybridization and introgression can lead to between species Wolbachia spread. In this way (and others), our work on local adaptation and reproductive isolation overlaps nicely with our work on Wolbachia spread.
We are currently funded by the National Institutes of Health (NIH) to determine the effects of Wolbachia on host physiology and fitness that enable Wolbachia spread. We are grateful for this funding and for past funding from the NIH, the National Science Foundation, and several other agencies.