How do oomycete and fungal effectors enter host plant cells?

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Oomycete and fungal plant pathogens cause a number of very important diseases. Many of these pathogens can deliver proteins into the cytoplasm of their host cells to disable host immunity; these proteins are called effectors. The mechanism by which these proteins enter host cells is poorly understood. The investigators have shown that oomycete and fungal effector proteins can enter host cells without the aid of any pathogen-encoded machinery, but instead rely on short amino acid sequences in the N-termini called RXLR motifs. The investigators have discovered that the RXLR motifs can bind a class of membrane lipids called phosphoinositides. In this project, the investigators will test whether binding of the effectors to phosphoinositides is actually responsible for transferring the effectors into host cells. They will identify which host phosphoinositides are utilized by the effectors, and they will characterize the mechanism of binding. Finally they will test whether it is possible to block effector entry and so prevent disease. An extremely wide range of the most destructive plant pathogens, including those causing wheat rust, rice blast, grape powdery mildew and potato late blight depend on effectors. Understanding effector entry and determining how to block it would provide an entirely new approach to treating this broad class of diseases. Treatment of animal diseases caused by fungi, oomycetes and some parasites may also be treatable by this approach. This project will train two graduate students and provide summer research opportunities for multi-cultural undergraduate students.