Late blight pathogen targets host Rab-G3 GTPases with an atypical GTPase-activating protein.

Late blight pathogen Phytophthora infestans secretes numerous effectors to suppress plant immunity. However, little is known about their underlying biochemical mechanisms. Here we report that, in the host Nicotiana benthamiana, P. infestans core RXLR effector Pi17063 suppresses plant immunity by targeting the host plasma membrane and NbRab-G3 proteins, small GTPases of the Ras-related brain (Rab) family. Pi17063 functions as their specific GTPase-activating protein (GAP), driving them to the cytoplasm-localized guanosine diphosphate (GDP)-bound inactive state. Mutant analysis of the conserved Pi17063 arginine residues showed the essential role of its GAP activity for virulence contribution. All four NbRab-G3 subfamily members are positive immune regulators, and NbRab-G3c mutants lost the ability to switch between active and inactive states and showed compromised immune function. Consistent with this, both silencing and overexpression of an endogenous GAP, NbGYP, inhibited NbRab-G3c-mediated plant immunity. Our results revealed positive immune roles of host NbRab-G3 GTPases, the importance of their state balance, and the biochemical mechanism by which their functions are suppressed by a P. infestans effector, providing insights into understanding eukaryotic effector-mediated plant susceptibility.