Evolution and ecology of social immunity in termites 

Busy soldiers of Coptotermes gestroi

A fundamental yet seemingly contradictory aspect of biological individuals is their capacity to remain the same while changing through time [Pradeu, 2011]. This self-regulatory ability is facilitated by a number of factors that are shared by all complex multicellular life-forms. One such essential trait is an effective immune system. Here, we use concepts of individuality and immunity to explore the blurred line between society and individual in termite “superorganisms”. We exploit a range of termite species to investigate interactions and trade-offs between individual and social immunity. We are interested in externally secreted immune molecules (here), and are investigating how caste, in addition to behavioral (here) and physiological host responses interact with canonical immune components to shape social immunity. We are also interested in the evolution of immunity during the transition to eusociality, and we are investigating this in a comparative framework using representatives from solitary and subsocial cockroach lineages through to fully eusocial termites.

Previous research topics

Host-parasite interactions

DAPI and Phalloidin stains IPLs. Host cell nucleus: large blue structure. Microsporidia: small twin blue spots

Nature is complicated. Hosts and parasites do not interact in closed one-to-one systems. We looked at the issue of complex multi-host-pathogen dynamics by using the intracellular gut parasites of bees: Nosema (Phylum Microspora, once thought to be unusual protists, they are now known to be highly derived fungi). Microsporidia have evolved a unique and very impressive host-invasion strategy. Spores eject a filament that uncoils like a spring, the force of which pierces the host cell. We examined whether order of infection matters when two related Nosema species: Nosema ceranae (invasive in A. mellifera, pictured) and Nosema apis (native in A. mellifera) were competed against one another.

Evolution of virulence and disease emergence in bee pollinators

Honeybee forager (Apis mellifera)

We are interested in understanding how changes in selective pressures (e.g. host switching, other traits influencing virulence or transmission) affect genotypic and phenotypic evolution in pathogenic organisms. Many serious disease threats to humans and wildlife are exposed to environmental perturbations (such as climate change and host or vector range expansion), resulting in rapid but potentially sustained shifts in selection on pathogens. How do pathogenic organisms adapt to selection, and how does this impact the likelihood of disease emergence? We are seeking to address this question by using rapidly evolving RNA viruses in bee pollinators. We have recently shown the wider risk of emerging infectious diseases to managed and wild (e.g. bumble bees) pollinators, and have demonstrated that an emerging strain of one of the more serious viruses associated with honeybee decline, Deformed wing virus, is more virulent than the globally established variant.

Parasitism, molecular evolution and species diversity 

Free-flying male (bottom right) and an endoparastic female whose cephalothorax (arrow) extrudes from the cuticle of a cricket host. The male is about 2 mm in length and the cricket about 10 mm.

Here, we examined whether being a parasite impacted the rate of evolution. We used the parasitic order Strepsiptera (the ‘twisted-wing parasites’) as a model to investigate this issue. Strepsiptera also contain an unusual lineage (Myrmecolacidae: pictured below), wherein males and females of the same species infect different host species. Males typically parasitize ants, while females parasitize crickets or preying mantises. We investigated whether this very unusual relationship influenced the history of diversification.