Host-Mediated S-Nitrosylation Disarms the Bacterial Effector HopAI1 to Reestablish Immunity

Pathogens deliver effectors into plant cells to suppress immunity-related signaling. However, effector recognition by the host elicits a hypersensitive response (HR) that overcomes the inhibition of host signaling networks, restoring disease resistance. Signaling components are shared between the pathogen-associated molecular pattern-triggered immunity and effector-triggered immunity, and it is unclear how plants inactivate these effectors to execute the HR. Here, we report that, in Arabidopsis thaliana , during the onset of the HR, the bacterial effector HopAI1 is S -nitrosylated and that this modification inhibits its phosphothreonine lyase activity. HopAI1 targets and suppresses mitogen-activated protein kinases (MAPKs). The S -nitrosylation of HopAI1 restores MAPK signaling and is required during the HR for activation of the associated cell death. S -nitrosylation is therefore revealed here as a nitric oxide-dependent host strategy involved in plant immunity that works by directly disarming effector proteins.