Key Laboratory of Plant Molecular Physiology, CAS Center for Excellence in Molecular Plant Sciences, Institute of Botany, Chinese Academy of Sciences, Beijing 100093, China; University of Chinese Academy of Sciences, Beijing 100049, China.
Key Laboratory of Plant Molecular Physiology, CAS Center for Excellence in Molecular Plant Sciences, Institute of Botany, Chinese Academy of Sciences, Beijing 100093, China; School of Life Sciences, Qilu Normal University, Jinan 250200, China.
Mol Plant. 2019 Jul 1;12(7):967-983. doi: 10.1016/j.molp.2019.03.012. Epub 2019 Apr 1.
Plants utilize intracellular nucleotide-binding leucine-rich repeat domain-containing receptors (NLRs) to recognize pathogen effectors and induce a robust defense response named effector-triggered immunity (ETI). The Arabidopsis NLR protein HOPZ-ACTIVATED RESISTANCE 1 (ZAR1) forms a precomplex with HOPZ-ETI-DEFICIENT 1 (ZED1), a receptor-like cytoplasmic kinase (RLCK) XII-2 subfamily member, to recognize the Pseudomonas syringae effector HopZ1a. We previously described a dominant mutant of Arabidopsis ZED1, zed1-D, which displays temperature-sensitive autoimmunity in a ZAR1-dependent manner. Here, we report that the RLCKs SUPPRESSOR OF ZED1-D1 (SZE1) and SZE2 associate with the ZAR1-ZED1 complex and are required for the ZED1-D-activated autoimmune response and HopZ1a-triggered immunity. We show that SZE1 but not SZE2 has autophosphorylation activity, and that the N-terminal myristoylation of both SZE1 and SZE2 is critical for their plasma membrane localization and ZED1-D-activated autoimmunity. Furthermore, we demonstrate that SZE1 and SZE2 both interact with ZAR1 to form a functional complex and are required for resistance against P. syringae pv. tomato DC3000 expressing HopZ1a. We also provide evidence that SZE1 and SZE2 interact with HopZ1a and function together with ZED1 to change the intramolecular interactions of ZAR1, leading to its activation. Taken together, our results reveal SZE1 and SZE2 as critical signaling components of HopZ1a-triggered immunity.
植物利用细胞内核苷酸结合富含亮氨酸重复结构域受体（NLRs）识别病原体效应物，并诱导一种称为效应物触发免疫（ETI）的强大防御反应。拟南芥 NLR 蛋白 HOPZ-ACTIVATED RESISTANCE 1（ZAR1）与受体样细胞质激酶（RLCK）XII-2 亚家族成员 HOPZ-ETI-DEFICIENT 1（ZED1）形成预复合物，以识别丁香假单胞菌效应物 HopZ1a。我们之前描述了拟南芥 ZED1 的显性突变体 zed1-D，它以 ZAR1 依赖的方式表现出温度敏感的自身免疫。在这里，我们报告 RLCKs SUPPRESSOR OF ZED1-D1（SZE1）和 SZE2 与 ZAR1-ZED1 复合物相关联，并且对于 ZED1-D 激活的自身免疫反应和 HopZ1a 触发的免疫是必需的。我们表明，SZE1 而不是 SZE2 具有自身磷酸化活性，并且 SZE1 和 SZE2 的 N 端豆蔻酰化对于它们在质膜上的定位和 ZED1-D 激活的自身免疫是关键的。此外，我们证明 SZE1 和 SZE2 均与 ZAR1 相互作用以形成功能性复合物，并且对于表达 HopZ1a 的丁香假单胞菌 pv.番茄 DC3000 具有抗性是必需的。我们还提供了证据表明 SZE1 和 SZE2 与 HopZ1a 相互作用，并与 ZED1 一起共同改变 ZAR1 的分子内相互作用，导致其激活。总之，我们的结果揭示了 SZE1 和 SZE2 是 HopZ1a 触发免疫的关键信号成分。
