- Associate Professor
My empirical work explores the interactions between Drosophila species and their symbionts (nematodes, bacteria and viruses) as well as meiotic drive elements. Recent developments in sequencing technology and bioinformatics have made it possible to address questions in evolutionary genetics and genomics in novel ways.
Immunity genes are among the fastest evolving genes in several animal taxa. This is consistent with theoretical predictions that both hosts and parasites are constantly evolving in response to newly acquired adaptations of the other – an evolutionary arms race. It is surprising, therefore, that antimicrobial peptides (AMPs) – small, secreted proteins that interact directly with pathogens – are generally not fast evolving in insects. This, along with patterns of gene gain and loss and association mapping led several researchers to propose that AMPs exhibit considerable functional redundancy and at the individual level are under weak selection and have little influence on immune response. In a recent genome-wide association study, we found a single nucleotide polymorphism in the antimicrobial peptide, Diptericin, that challenges this idea. The SNP was among the most significantly associated with bacterial load 24 hours after infection with Providencia rettgeri, a natural pathogen of D. melanogaster. Two lines used in the study carried an allele that resulted in a premature stop codon in Diptericin and these two lines had the absolute highest bacterial load 24 hours post infection. Furthermore, the same amino acid polymorphism exists in D. simulans through a case of convergence using a different codon. The same phenotypic effect exists in D. simulans as well. These results challenge the current dogma about AMPs in insects and suggest several new lines of inquiry regarding their evolution.
Gene family expansion through duplication has long been recognized as a means of generating evolutionary novelty though the evolutionary processes leading from gene duplication to novel function is not well established. One striking characteristic of the evolution of AMPs is the high rate of gene duplication in AMP gene families. We are using duplications in AMP gene families to better understand both AMP function and the evolution of gene duplication. The ability to perform high throughput experiments and genetic manipulations in Drosophila and the existence of a set of expected phenotypes involved in AMP function make the system tractable.
We recently discovered Drosophila innubila Nudivirus (DiNV), the first DNA virus associated with Drosophila, that infects several species from across the genus in North America (Unckless 2011). A similar virus was recently found in Drosophila collected in Europe and Africa. The virus is a double-stranded circular DNA virus from the relatively poorly characterized Nudivirus family. The closest relative of DiNV infects the rhinoceros beetle (Oryctes rhinoceros) and has been used as a biological control agent for decades. Two species, which are sister to each other but are allopatric (D. falleni in temperate Northern environments and D. innubila in the Sky Islands of the Southwest), carry strains of the virus that show about five percent nucleotide divergence. In both species, the virus is found at considerable frequency in wild-caught flies (up to 40 %) and cause significant reduction in fertility and survivorship. We are working to get the virus growing in cell culture so that we can understand its virulence, host range and evolution.
Sex-ratio meiotic drive
Our other major area of empirical research is a genomic and population level analysis of the Drosophila affinis meiotic drive system. Sex-ratio males, those carrying a driving X chromosome, sire nearly all daughters because the driving X disables Y-bearing sperm. Important work by Robert Voelker and colleagues in the 1960s and 1970s found that a) XO males (those lacking a Y) are fertile, b) a driving X chromosome produces nearly all daughters when in XY males, but nearly all females when in XO males, c) the Y outcompetes the O in the absence of the driving X, and d) a second driving X is not suicidal when paired with the O, but drive is much weaker. We aim to elucidate the genomic basis of drive and monitor long-term population dynamics of the two drivers and the Y/O polymorphism.
As stated above, I am interested in how conflict shapes ecological and evolutionary processes. My theory work in this area has recently focused on sex-ratio meiotic drive and synthetic gene drive. To date I have looked at the effect of meiotic drive on population extinction, speciation and sex-chromosome evolution (discussed above).