Two Arabidopsis Receptor-like Cytoplasmic Kinases SZE1 and SZE2 Associate with the ZAR1-ZED1 Complex and Are Required for Effector-Triggered Immunity
文献类型:期刊论文
作者 | Liu, Cheng7; Cui, Dayong6; Zhao, Jingbo; Liu, Na5; Wang, Bo4; Liu, Jing; Xu, Enjun; Hu, Zhubing3; Ren, Dongtao4; Tang, Dingzhong5 |
刊名 | MOLECULAR PLANT |
出版日期 | 2019 |
卷号 | 12期号:7页码:967-983 |
ISSN号 | 1674-2052 |
关键词 | Arabidopsis RLCK SZE-ZAR1-ZED1 complex HopZ1a immune response |
DOI | 10.1016/j.molp.2019.03.012 |
文献子类 | Article |
英文摘要 | 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. |
学科主题 | Biochemistry & Molecular Biology ; Plant Sciences |
电子版国际标准刊号 | 1752-9867 |
出版地 | CAMBRIDGE |
WOS关键词 | DISEASE RESISTANCE PROTEIN ; FLAX RUST ; PLANT ; ACTIVATION ; RECOGNITION ; PERCEPTION ; FAMILY ; DOMAIN ; MYRISTOYLATION ; BIOSYNTHESIS |
WOS研究方向 | Biochemistry & Molecular Biology ; Plant Sciences |
语种 | 英语 |
出版者 | CELL PRESS |
WOS记录号 | WOS:000473296400007 |
资助机构 | National Natural Science Foundation of ChinaNational Natural Science Foundation of China (NSFC) [31471160] ; Strategic Priority Research Program of Chinese Academy of SciencesChinese Academy of Sciences [XDB27030102] |
源URL | [http://ir.ibcas.ac.cn/handle/2S10CLM1/19546] |
专题 | 中科院植物分子生理学重点实验室 |
作者单位 | 1.Natl Ctr Plant Gene Res, Beijing 100093, Peoples R China 2.Henan Univ, Dept Biol, State Key Lab Cotton Biol, Inst Plant Stress Biol, Kaifeng 475001, Peoples R China 3.China Agr Univ, Coll Biol Sci, State Key Lab Plant Physiol & Biochem, Beijing 100193, Peoples R China 4.Fujian Agr & Forestry Univ, Plant Immun Ctr, Minist Educ Genet Breeding & Multiple Utilizat Cr, Key Lab, Fuzhou 350002, Peoples R China 5.Qilu Normal Univ, Sch Life Sci, Jinan 250200, Shandong, Peoples R China 6.Univ Chinese Acad Sci, Beijing 100049, Peoples R China 7.Chinese Acad Sci, Key Lab Plant Mol Physiol, CAS Ctr Excellence Mol Plant Sci, Inst Bot, Beijing 100093, Peoples R China |
推荐引用方式 GB/T 7714 | Liu, Cheng,Cui, Dayong,Zhao, Jingbo,et al. Two Arabidopsis Receptor-like Cytoplasmic Kinases SZE1 and SZE2 Associate with the ZAR1-ZED1 Complex and Are Required for Effector-Triggered Immunity[J]. MOLECULAR PLANT,2019,12(7):967-983. |
APA | Liu, Cheng.,Cui, Dayong.,Zhao, Jingbo.,Liu, Na.,Wang, Bo.,...&Hu, Yuxin.(2019).Two Arabidopsis Receptor-like Cytoplasmic Kinases SZE1 and SZE2 Associate with the ZAR1-ZED1 Complex and Are Required for Effector-Triggered Immunity.MOLECULAR PLANT,12(7),967-983. |
MLA | Liu, Cheng,et al."Two Arabidopsis Receptor-like Cytoplasmic Kinases SZE1 and SZE2 Associate with the ZAR1-ZED1 Complex and Are Required for Effector-Triggered Immunity".MOLECULAR PLANT 12.7(2019):967-983. |
入库方式: OAI收割
来源:植物研究所
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