The receptor-like cytoplasmic kinase RIPK regulates broad-spectrum ROS signaling in multiple layers of plant immune system
The receptor-like cytoplasmic kinase RIPK regulates broad-spectrum ROS signaling in multiple layers of plant immune system
复制标题
受体样细胞质激酶 RIPK 调节植物免疫系统多层中的广谱 ROS 信号传导
DOI：
10.1016/j.molp.2021.06.010
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发表时间：
2021-10-04
期刊：
影响因子：
27.5
通讯作者：
Liang, Yan
中科院分区：
文献类型：
--
作者：
Li, Ping;Zhao, Lulu;Liang, Yan
通过呼吸爆发氧化酶同系物（RBOH）的活性产生活性氧（ROS）在植物免疫系统的多个层次中起重要作用，包括病原相关分子模式触发免疫（PTI）、损伤相关分子模式触发免疫（DTI）、效应物触发免疫（ETI）和系统获得性抗性（SAR）。一般认为，RBOHD是由不同的受体样细胞质激酶（RLCK）激活，以响应各种免疫激发子。在这项研究中，我们发现RPM 1诱导的蛋白激酶（RIPK），RLCK VII亚家族成员，有助于在植物免疫系统的多个层次中产生ROS。ripk突变体显示响应于用所有检测的触发PTI、DTI、ETI和SAR的免疫诱导剂处理的ROS产生减少。我们发现RIPK在体外可以直接磷酸化RBOHD的N端区域，并且在所有测试的免疫激发子处理后，RBOHD的磷酸化S343/S347残基的水平在ripk突变体中显著低于野生型。我们进一步证明了RIPK的磷酸化是其调节RBOHD介导的ROS产生的功能所必需的。类似rbohd，ripk突变体表现出气孔关闭减少和受损的SAR，并容易受到necrotrophic细菌Pectobacterium carotovorum。总的来说，我们的研究结果表明，RIPK调节广谱RBOHD介导的ROS信号在PTI，DTI，ETI和SAR，导致随后的RBOHD依赖性免疫反应。
Production of reactive oxygen species (ROS) via the activity of respiratory burst oxidase homologs (RBOHs) plays a vital role in multiple layers of the plant immune system, including pathogen-associated molecular pattern-triggered immunity (PTI), damage-associated molecular pattern-triggered immunity (DTI), effector-triggered immunity (ETI), and systemic acquired resistance (SAR). It is generally established that RBOHD is activated by different receptor-like cytoplasmic kinases (RLCKs) in response to various immune elicitors. In this study, we showed that RPM1-INDUCED PROTEIN KINASE (RIPK), an RLCK VII subfamily member, contributes to ROS production in multiple layers of plant immune system. The ripk mutants showed reduced ROS production in response to treatment with all examined immune elicitors that trigger PTI, DTI, ETI, and SAR. We found that RIPK can directly phosphorylate the N-terminal region of RBOHD in vitro, and the levels of phosphorylated S343/S347 residues of RBOHD are sigfniciantly lower in ripk mutants compared with the wild type upon treatment with all tested immune elicitors. We further demonstrated that phosphorylation of RIPK is required for its function in regulating RBOHD-mediated ROS production. Similar to rbohd, ripk mutants showed reduced stomatal closure and impaired SAR, and were susceptible to the necrotrophic bacterium Pectobacterium carotovorum. Collectively, our results indicate that RIPK regulates broad-spectrum RBOHD-mediated ROS signaling during PTI, DTI, ETI, and SAR, leading to subsequent RBOHD-dependent immune responses.