Molecular arms-races and the evolution of immune genes
We are interested understanding how gene function determines the rate of adaptive evolution, and particularly whether molecular 'arms-races' drive a disproportionate amount of adaptive substitution. Because the immune system coevolves with pathogens (and other parasites), it is expected to evolve rapidly relative to the rest of the genome, and we have used population genetics approaches in Drosophila to look for differences in the rate of adaptive evolution between immunity and non-immunity genes, and between different types of immunity gene. In Drosophila it is striking that RNAi genes (including those that defend against viruses) show very strong evidence of adaptive evolution, suggesting that they are engaged in a host-parasite arms race with viruses. To understand whether this is peculiar to Drosophila, we are now asking similar questions using a population-genomic study of Daphnia magna, in collaboration with Tom Little.
Although Drosophila is one of our best models for innate immunity, we know surprisingly little about its natural pathogens. Viruses are common in Drosophila and seem to be a major driver of evolution in its immune system. However, so far only a handful have been studied in the lab, and apart from the Sigma rhabdovirus (see The Jiggins Lab) none have been widely studied in the wild. By discovering new Drosophila viruses, and by studying the prevalence, population history, and molecular evolution of known viruses, we can provide a sound evolutionary context for understanding anti-viral immunity in invertebrates.
The evolution of RNAi
RNA interference has an essential role in mediating defence against viruses and transposable elements. This is well-studied in plants, nematodes and insects, and appears to be phylogenetically ancient. I have a broad interest in the phylogenetic origins of defensive RNAi, and particularly in the relative roles that viruses and transposable elements have played in shaping the extant RNAi pathways in insects.