Plants utilize nucleotide-binding, leucine-rich repeat receptors (NLRs) to detect pathogen effectors, leading to effector-triggered immunity. The NLR ZAR1 indirectly recognizes the Xanthomonas campestris pv. campestris effector AvrAC and Pseudomonas syringae effector HopZ1a by associating with closely related receptor-like cytoplasmic kinase subfamily XII-2 (RLCK XII-2) members RKS1 and ZED1, respectively. ZAR1, RKS1, and the AvrAC-modified decoy PBL2^UMP form a pentameric resistosome in vitro, and the ability of resistosome formation is required for AvrAC-triggered cell death and disease resistance. However, it remains unknown whether the effectors induce ZAR1 oligomerization in the plant cell. In this study, we show that both AvrAC and HopZ1a can induce oligomerization of ZAR1 in Arabidopsis protoplasts. Residues mediating ZAR1–ZED1 interaction are indispensable for HopZ1a-induced ZAR1 oligomerization in vivo and disease resistance. In addition, ZAR1 residues required for the assembly of ZAR1 resistosome in vitro are also essential for HopZ1a-induced ZAR1 oligomerization in vivo and disease resistance. Our study provides evidence that pathogen effectors induce ZAR1 resistosome formation in the plant cell and that the resistosome formation triggers disease resistance.

植物利用核苷酸结合的富含亮氨酸的重复受体（NLR）来检测病原体效应物，从而导致效应物触发的免疫力。NLR ZAR1间接识别Xanthomonas campestris pv。油菜效应AvrAC和丁香假单胞菌的效应HopZ1a通过与关联密切相关的受体样激酶胞质分别亚科XII-2（RLCK XII-2）的成员RKS1和ZED1。ZAR1，RKS1和AvrAC修饰的诱饵PBL2 ^UMP在体外形成五聚体抗脂质体，并且抗脂质体形成的能力是AvrAC触发的细胞死亡和疾病抵抗所必需的。然而，尚不清楚效应子是否在植物细胞中诱导ZAR1寡聚。在这项研究中，我们表明AvrAC和HopZ1a都可以诱导拟南芥原生质体中ZAR1的寡聚。介导ZAR1-ZED1相互作用的残基对于HopZ1a诱导的ZAR1体内寡聚化和抗病性是必不可少的。此外，在体外组装ZAR1抵抗小体所需的ZAR1残基对于HopZ1a诱导的ZAR1体内寡聚化也是必不可少的和疾病抵抗力。我们的研究提供了证据，表明病原体效应物诱导了植物细胞中ZAR1抵抗小体的形成，并且抵抗小体的形成触发了疾病抗性。