Genetic and biochemical bases of fungal nonself recognition

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My NSERC Program investigates the biochemical and genetic bases of nonself recognition in fungi, a process that is analogous to graft rejection in animals and plants. Similar to "more complex organisms", fungi use nonself recognition systems to slow or prevent disease transmission (and thus thwart biological control programs), and to modulate intra- and interspecies interactions, including interactions involved in the maintenance of territory. At the biochemical level, our research will investigate how nonself recognition proteins interact to trigger a phenomenon called Programmed Cell Death (PCD). PCD is one way that organisms limit their own proliferation, and thus understanding this process has applications in diverse areas such as in developing control strategies for pathogens of plants and animals. We have evidence that nonself recognition proteins trigger PCD by sticking together to form a toxic complex, and that protein degradation can rid the cell of such complexes. Similar protein degradation processes are central to diseases associated with prion-like elements such as Huntington's and Bovine Spongiform Encephalopathy (BSE, "Mad Cow Disease"). At the genetic level we will clone and characterize additional nonself recognition genes to gain an understanding of the diversity of factors that fungi use for nonself recognition. Finally, we will determine how naturally occurring viruses manipulate nonself recognition systems to gain access to their fungal host. Our exploration of the interaction between viruses and incompatibility factors is relevant to diverse areas of host - parasite interactions and may lead to improved biological control strategies for plant pathogens. Overall, the proposed research into nonself recognition will significantly enhance our understanding of this basic biological phenomenon and will provide advanced training to students in a variety of highly desirable fields such as genetics, microbiology and biochemistry.