Research
My central thesis is that sex determination diversification is, in part, driven by heritable male-killing (MK) symbionts. Based on my findings to date, I argue that symbionts target sex-specific signals to kill male hosts – and in doing so drive hosts to change the way sex is defined to avoid the MK action. For the hypothesis to be broadly true, male-killers would deploy more diverse mechanisms (causative genes), and hosts, as a result, would have diverse evolved responses within the sex determination cascade.
Evolution of the male-killing trait across symbionts and host species
One of my main research interests is how convergent evolution has shaped the mechanistic diversity of male killing. During my Ph.D. at the Tokyo University of Agriculture and Technology and my postdoctoral research at the National Agriculture and Food Research Organisation in Japan, I developed both in vivo and in vitro systems to study the effects of male-killing microbes. This work showed that taxonomically distant male killers - including bacteria from different genera and viruses - have evolved distinct mechanisms to eliminate male hosts. I also demonstrated that a single bacterial symbiont, Wolbachia, can induce male killing through different mechanisms driven by distinct causative genes. These mechanisms are closely linked to host sex determination cascades. Building on these findings, my current research at the University of Liverpool focuses on the molecular interactions between male-killing symbionts and insect sex determination systems, and how male killing may, in turn, drive the evolution of these systems.
Escalating arms races between male killers and host insects
Male killing can impose significant fitness costs on the host, and natural selection favours host mutations that suppress the action of the symbiont. A key question is whether male killing can re-emerge in response to host suppression. My recent research demonstrates the evolution of a Wolbachia variant that induces male killing despite the presence of a circulating suppressor in a butterfly host. Through collaborative work in Asia and Europe, I showed that one Wolbachia strain was sensitive to the host suppressor, while a closely related strain carrying an additional prophage element was unaffected by suppression. These findings suggest an escalating evolutionary arms race between male-killing symbionts and their hosts, with bacteriophages playing a pivotal role in the adaptation of male-killing bacteria. Building on these insights, I am currently investigating the genetic and mechanistic basis of suppression, as well as the contrasting dynamics of suppressed and unsuppressed male-killing phenotypes.
Research collaborations
Daisuke Kageyama
NARO
I collaborate with Dr Daisuke Kageyama on a range of projects developing a study system in the field of symbiosis and selfish genetic elements. Our ongoing and previous work has been supported by the Japan Society for the Promotion of Science (JSPS).