In plant immunity, phosphatidic acid (PA) regulates reactive oxygen species (ROS) by binding to respiratory burst oxidase homolog D (RBOHD), an NADPH oxidase responsible for ROS production. Here, we analyze the influence of PA binding on RBOHD activity and the mechanism of RBOHD-bound PA generation. PA binding enhances RBOHD protein stability by inhibiting vacuolar degradation, thereby increasing chitin-induced ROS production. Mutations in diacylglycerol kinase 5 (DGK5), which phosphorylates diacylglycerol to produce PA, impair chitin-induced PA and ROS production. The transcript (but not α) complements reduced PA and ROS production in mutants, as well as resistance to . Phosphorylation of S506 residue in the C-terminal calmodulin-binding domain of DGK5β contributes to the activation of DGK5β to produce PA. These findings suggest that DGK5β-derived PA regulates ROS production by inhibiting RBOHD protein degradation, elucidating the role of PA-ROS interplay in immune response regulation.

中文翻译：

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DGK5β 衍生的磷脂酸通过稳定 NADPH 氧化酶来调节植物免疫中 ROS 的产生

在植物免疫中，磷脂酸 (PA) 通过与呼吸爆发氧化酶同系物 D (RBOHD)（一种负责 ROS 产生的 NADPH 氧化酶）结合来调节活性氧 (ROS)。在这里，我们分析了 PA 结合对 RBOHD 活性的影响以及 RBOHD 结合的 PA 生成机制。PA 结合通过抑制液泡降解来增强 RBOHD 蛋白稳定性，从而增加几丁质诱导的 ROS 产生。二酰甘油激酶 5 (DGK5) 磷酸化二酰甘油产生 PA，其突变会损害几丁质诱导的 PA 和 ROS 产生。转录本（但不是 α）补充了突变体中 PA 和 ROS 产生的减少，以及对 . DGK5β C 端钙调蛋白结合域中 S506 残基的磷酸化有助于激活 DGK5β 产生 PA。这些发现表明，DGK5β 衍生的 PA 通过抑制 RBOHD 蛋白降解来调节 ROS 产生，阐明了 PA-ROS 相互作用在免疫反应调节中的作用。