Two Arabidopsis Receptor-Like Cytoplasmic Kinases SZE1 and SZE2 Associate with the ZAR1-ZED1 Complex and Are Required for Effector-Triggered Immunity.

Research paper by Cheng C Liu, Dayong D Cui, Jingbo J Zhao, Na N Liu, Bo B Wang, Jing J Liu, Enjun E Xu, Zhubing Z Hu, Dongtao D Ren, Dingzhong D Tang, Yuxin Y Hu

Indexed on: 06 Apr '19Published on: 05 Apr '19Published in: Molecular Plant


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 the HOPZ-ETI-DEFICIENT1 (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, that 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 or SZE2 interacts with ZAR1 to form a functional complex and is required for the resistance against P. syringae pv. tomato DC3000 expressing HopZ1a. We also provide the evidence that SZE1 and SZE2 interact with HopZ1a and function together with ZED1 to change the intramolecular interactions of ZAR1 for its activation. Taken together, our results reveal the SZE1 and SZE2 as critical signaling components of HopZ1a-triggered immunity. Copyright © 2019 The Author. Published by Elsevier Inc. All rights reserved.