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的富含亮氨酸的重复域含受体（NLR）识别病原体效应子并诱导强大的防御反应，称为效应子触发的免疫（ETI）。的拟南芥NLR蛋白HOPZ活化抗性1（ZAR1）形成与HOPZ-ETI缺陷1（ZED1），受体样细胞质激酶（RLCK）XII-2亚家族成员一个预复合，以识别丁香假单胞菌效应HopZ1a。我们先前描述的显性突变体拟南芥ZED1，zed1-d ，在ZAR1依赖性方式，其显示对温度敏感的自身免疫。在这里，我们报告ZED1-D1（SZE1）和SZE2的RLCKs抑制子与ZAR1-ZED1复合体相关，是ZED1-D激活的自身免疫反应和HopZ1a触发的免疫所必需的。我们显示，SZE1但不是SZE2具有自磷酸化活性，并且SZE1和SZE2的N末端肉豆蔻酰化对其质膜定位和ZED1-D激活的自身免疫性至关重要。此外，我们证明SZE1和SZE2都与ZAR1相互作用形成功能复合物，并且是抵抗P的必需物质。丁香科植物 番茄表示HopZ1a的DC3000。我们还提供证据表明SZE1和SZE2与HopZ1a相互作用，并与ZED1一起起作用以改变ZAR1的分子内相互作用，从而导致其活化。两者合计，我们的结果表明SZE1和SZE2是HopZ1a触发的免疫的关键信号组成部分。