Department of Biotechnology, University of Verona, Verona 37134, Italy.
Department of Biotechnology, University of Verona, Verona 37134, Italy
Plant Cell. 2017 Nov;29(11):2871-2881. doi: 10.1105/tpc.16.00557. Epub 2017 Oct 30.
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 , during the onset of the HR, the bacterial effector HopAI1 is -nitrosylated and that this modification inhibits its phosphothreonine lyase activity. HopAI1 targets and suppresses mitogen-activated protein kinases (MAPKs). The -nitrosylation of HopAI1 restores MAPK signaling and is required during the HR for activation of the associated cell death. -nitrosylation is therefore revealed here as a nitric oxide-dependent host strategy involved in plant immunity that works by directly disarming effector proteins.
病原体将效应物输送到植物细胞中以抑制与免疫相关的信号转导。然而，宿主对效应物的识别会引发超敏反应 (HR)，从而克服宿主信号网络的抑制，恢复抗病性。信号成分在病原体相关分子模式触发的免疫和效应物触发的免疫之间共享，目前尚不清楚植物如何使这些效应物失活以执行 HR。在这里，我们报告说，在 中，在 HR 开始时，细菌效应物 HopAI1 被 - 亚硝化，并且这种修饰抑制其磷酸苏氨酸裂合酶活性。HopAI1 靶向并抑制丝裂原活化蛋白激酶 (MAPKs)。HopAI1 的 - 亚硝化恢复了 MAPK 信号转导，并且在 HR 期间对于相关细胞死亡的激活是必需的。因此，这里揭示了 - 亚硝化作为一种依赖于一氧化氮的宿主策略，参与植物免疫，其作用是通过直接解除效应蛋白的功能来实现的。
