3 years ago

Host-mediated S-nitrosylation disarms the bacterial effector HopAI1 to re-establish immunity.

Elodie Vandelle, Tengfang Ling, Massimo Delledonne, Diana Bellin, Zahra Imanifard
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 (PAMP)-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 (NO)-dependent host strategy involved in plant immunity that works by directly disarming effector proteins.

Publisher URL: http://doi.org/10.1105/tpc.16.00557

DOI: 10.1105/tpc.16.00557

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