Environmental and genetic orchestration of fungal zinc-scavenging systems

Determining how human fungal pathogens have evolved to be able to infect their hosts is critical to understanding their emergence and spread. Our group studies a molecule called Pra1 which fungi produce to capture the essential mineral zinc from their environment. However the Pra1 molecule also causes inflammation in the human body. Interestingly, several fungal pathogens have lost the Pra1 gene during their evolution. We have recently shown that the Pra1 status of fungal pathogens strongly influences their capacity to cause inflammation; this is important because inflammation can either benefit the human body, by helping to clear the infection, or damage it, via an adverse reaction called immunopathology. This project will examine how the local environment faced by fungi influences the regulation and ultimately the evolution of the Pra1 gene in two major human fungal pathogens. As well as furthering our understanding of zinc capture by fungi, the project will provide broad information on how human fungal pathogens have evolved.