Bacterial Effectors Induce Oligomerization of Immune Receptor ZAR1 In Vivo

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 HopZIa 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 PBL2ump 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 HopZ1 a can induce oligomerization of ZAR1 in Arabidopsis protoplasts.Residues mediating ZAR1-ZED1 interaction are indispensable for HopZIa-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 HopZIa-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.