1. Host-Mediated S -Nitrosylation Disarms the Bacterial Effector HopAI1 to Reestablish Immunity.
- Author
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Ling T, Bellin D, Vandelle E, Imanifard Z, and Delledonne M
- Subjects
- Arabidopsis immunology, Arabidopsis microbiology, Arabidopsis Proteins metabolism, Cell Death, Disease Resistance immunology, Host-Pathogen Interactions, MAP Kinase Signaling System, Mitogen-Activated Protein Kinases metabolism, Plant Diseases immunology, Plant Diseases microbiology, Pseudomonas syringae physiology, Arabidopsis metabolism, Bacterial Proteins metabolism, Nitric Oxide metabolism, Pseudomonas syringae metabolism
- Abstract
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., (© 2017 American Society of Plant Biologists. All rights reserved.)
- Published
- 2017
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