Cleavage of BAK1 by a Pseudomonas syringae effector to subvert plant innate immunity.
L. LEI (1), K. Panya (2), Y. Liping (1), C. Gaihong (3), C. She (3), A. James (4), Z. Jian-Min (1) (1) State Key Laboratory of Plant Genomics, Institute of Genetics and Developmental Biology, CAS, China; (2) Center for Plant Science Innovation and School of Biological Sciences, University of Nebraska, Lincoln, NE, USA, U.S.A.; (3) National Institute of Biological Sciences, Beijing, China; (4) Center for Plant Science Innovation and Department of Plant Pathology, University of Nebraska, Lincoln, NE, USA, U.S.A.

The Arabidopsis immunity is activated by pattern-recognition receptors such as FLS2, which along with its co-receptor BAK1 perceives the bacterial flagellin epitope flg22. Phytopathogenic bacteria can inject a repertoire of effector proteins into host cells to aid in parasitism by perturbing pattern-triggered immunity. However, a major dilemma for phytopathogens is that the effector-induced perturbation often can be sensed by the host and trigger another layer of immunity as a result of plant-pathogen co-evolution. We report that the Pseudomonas syringae type III effector HopB1 acts as a novel protease to cleave BAK1 in an flg22-dependent manner. Prior to activation by flg22, HopB1 constitutively interacts with FLS2. The flg22-inducd recruitment and phosphorylation of BAK1 allows HopB1 to specifically cleave BAK1 between Arg297 and Gly298 to inhibit FLS2 signaling. Substitution of Arg297 with Ala leads to BAK1-mediated immune signaling that is insensitive to HopB1. Although perturbation of BAK1 is known to trigger increased immune responses in plants, the HopB1-mediated cleavage of immune-activated BAK1 leads to enhanced virulence but not disease resistance. This study thus reveals a unique virulence strategy by which a pathogen effector attacks the plant immune system with minimal host perturbation.

Abstract Number: P9-277
Session Type: Poster