Undermining effector-targeted susceptibility factors to provide late blight resistance

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An increasing world population and impacts of climate change place ever-greater demands on the world food supply. A major constraint to global food security is crop loss due to plant pests and diseases. With the increasing stringency of conditions under which chemicals are approved for agriculture, the choice of effective fungicides and pesticides will become more limited in the near future. Furthermore, as introgressed host resistance genes are rapidly defeated by pathogens and pests in the field, there is an urgent need to explore the development of novel, durable and sustainable means to combat crop diseases.Plants face a barrage of microbial threats and defend themselves by employing two layers of inducible defence responses. The first involves recognition by cell surface receptors of essential, widely conserved molecules (called PAMPs) that are exposed by pathogens during infection. Successful (adapted) pathogens secrete and deliver proteins called effectors to suppress these defences. The second defence layer involves recognition of effectors by immune receptors, resistance proteins, to evoke effector-triggered immunity. This project focusses on the late blight pathogen Phytophthora infestans, the major pathogen of potato and tomato, two of the world's main food crops. Amongst the weapons P. infestans has to subjugate its hosts are RXLR effectors which are delivered inside plant cells to promote susceptibility. RXLR effectors have been shown to target and suppress positive regulators of immunity. In contrast, here we present considerable unpublished information revealing the discovery of two RXLR effectors that target host susceptibility (S) factors; proteins whose activity promotes disease. One effector interacts with isoforms of plant protein phosphatase 1 (PP1), forming holoenzymes that may dephosphorylate host proteins to activate or inactivate them. The other effector interacts with NRL, member of a family of plasma membrane-associated regulators of light signalling. NRL promotes susceptibility by suppressing immunity triggered by perception of a P. infestans PAMP. S factors present very attractive opportunities to undermine infection effectively and durably. For example, whereas a resistance protein imposes a selection pressure on a pathogen to alter or lose the cognate avirulence gene to evade detection, modification or conditional removal of an S factor imposes a far more challenging selection pressure, in that the associated host protein activity is required for infection. Critically, reducing endogenous levels of these S factors (PP1c isoforms and NRL) attenuates P. infestans infection, suggesting that combined reduction of both S factors may provide a durable strategy to combat late blight.Little is understood about how S factors promote disease. It is an emerging, exciting area of plant disease research, making our proposal timely. We will provide detailed understanding of 1) the virulence targets dephosphorylated by effector-PP1c holoenzymes, and the mechanistic consequences of dephosphorylation (objective 1); and 2) the means by which NRL suppresses PAMP-triggered immunity (objective 2). It will also reveal whether natural variants exist of these S factors that cannot be targeted by the associated effectors (objective 3C), implicating evolution of S factors to evade effector-mediated exploitation. These studies will provide novel insights into negative regulation of plant immunity. They also provide novel means with which to combat plant disease, and potato blight specifically.Industry is keen to exploit understanding of S factors as a durable means to provide disease resistance. This project, with industrial partner JR Simplot, will deliver novel approaches for pathogen-inducible removal of S factors to provide late blight resistance (objectives 3A; 3B).