Throughout their complex lifecycles apicomplexan parasites pass between different hosts and encounter vastly different environments, triggering developmental progression and infectivity. This allows for their survival and propagation. Without their ability to sense environmental cues the life cycle of parasites is interrupted and they cannot survive. 

Understanding the identity of environmental cues and the mechanisms parasites use to sense these remains one of the major gaps in our fundamental understanding of the pathogenesis across Apicomplexa. Furthermore, such signalling pathways offer a rich new source of drug and vaccine targets to prevent or treat infection. 

Our current efforts in this area lie in understanding how parasites sense environmental cues to activate and switch off motility to regulate host cell invasion. 

We utilise the powerful forward and reverse genetics and experimental tractability of Toxoplasma to understand the molecular basis of environmental sensing and signal transduction and how this process is conserved across apicomplexan species. 

Central to signal transduction and activation of invasion is Ca²⁺ signalling and we continue to develop and adapt tools to probe the nature of this pathway (for example, the use of genetically encoded biosensors). 

We are also interested in understanding how parasites produce the force required for motility and invasion. The actomyosin-based ‘glideosome’ drives parasite motility and consists of a myosin anchored to the parasite periphery by the glideosome associated protein (GAP) complex. The myosin is made up of an unusual ‘type XIV’ heavy chain - MyoA - bound by two light chains. 

We are interested in defining how the MyoA produces force to drive motility. Here we use a combination of structural biology, parasite molecular biology and biophysics to understand how force is produced to drive apicomplexan motility and therefore provide a foundation in which to develop new drugs that prevent motility and invasion.