The bacterial effector H op M 1 suppresses PAMP ‐triggered oxidative burst and stomatal immunity

Summary Successful pathogens counter immunity at multiple levels, mostly through the action of effectors. Pseudomonas syringae secretes c . 30 effectors, some of which have been shown to inhibit plant immunity triggered upon perception of conserved pathogen‐associated molecular patterns ( PAMP s). One of these is H op M 1, which impairs late immune responses through targeting the vesicle trafficking‐related A t MIN 7 for degradation. Here, we report that in planta expressed H op M 1 suppresses two early PAMP ‐triggered responses, the oxidative burst and stomatal immunity, both of which seem to require proteasomal function but are independent of A t MIN 7. Notably, a 14‐3‐3 protein, GRF 8/ A t MIN 10, was found previously to be a target of H op M 1 in vivo , and expression of H op M 1 mimics the effect of chemically and genetically disrupting 14‐3‐3 function. Our data further show that the function of 14‐3‐3 proteins is required for PAMP ‐triggered oxidative burst and stomatal immunity, and chemical‐mediated disruption of the 14‐3‐3 interactions with their client proteins restores virulence of a H op M 1‐deficient P . syringae mutant, providing a link between H op M 1 and the involvement of 14‐3‐3 proteins in plant immunity. Taken together, these results unveil the impact of H op M 1 on the PAMP ‐triggered oxidative burst and stomatal immunity in an A t MIN 7‐independent manner, most likely acting at the function of (a) 14‐3‐3 protein(s).