Poster
Qing Liu
Institute of Microbiology, Chinese Academy of Sciences
Beijing, Beijing, China
Wenxin Xing
Institute of Microbiology, Chinese Academy of Sciences
Beijing, Beijing, China (People's Republic)
Daniel Monino-Lopez
Plant Breeding, Wageningen University and Research
Wageningen, Gelderland, Netherlands
Jan Sklenar
The Sainsbury Laboratory
Norwich, England, United Kingdom
Frank L.H. Menke
The Sainsbury Laboratory
Norwich, England, United Kingdom
Jack Vossen
Wageningen University & Research
Wageningen, Gelderland, Netherlands
Jonathan D. G. Jones
Prof. Group leader
The Sainsbury Laboratory
Norwich, England, United Kingdom
Xiao Lin
corresponding author
Institute of Microbiology, Chinese Academy of Sciences, China
Plants possess a two-layer immune system comprising pattern-triggered immunity (PTI) and effector-triggered immunity (ETI). However, plant pathogens secrete effectors to subvert host immunity, a process known as effector-triggered susceptibility (ETS), yet the underlying mechanisms remain poorly understood. Previously, we identified R04373, a resistance protein from Solanum americanum, which specifically recognizes the Phytophthora infestans effector PITG_04373. However, R04373 does not confer effective resistance against P. infestans. We found that the nuclear localization signal (NLS) of R04373 is crucial for its function and that R04373 is associated with PITG_04373. To investigate how R04373-mediated immunity is compromised, we screened a P. infestans RXLR effector library and identified S04373, an effector that specifically suppresses the hypersensitive response (HR) triggered by R04373 and PITG_04373. Notably, S04373 also suppresses the Rpi-chc1 and R2-mediated HR. Further analysis revealed that S04373 inhibits ETI by targeting host importin α and β, which are essential components in the nuclear protein import pathway. These findings reveal that nuclear transport is indispensable for ETI activation and serves as a key target for pathogen effectors. Understanding the ETS mechanism will contribute to designing the plant immune system and restoring the impaired R genes.