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Pseudomonas syringae activates ZAT18 to inhibit salicylic acid accumulation by repressing EDS1 transcription for bacterial infection

文献类型： 外文期刊

作者： Gao, Yuhan 1 ; Li, Ze 1 ; Yang, Chenyu 1 ; Li, Guangyue 1 ; Zeng, Hongmei 1 ; Li, Zhonghai 2 ; Zhang, Yi 3 ; Yang, Xiufen 1 ;

作者机构： 1.Chinese Acad Agr Sci, Inst Plant Protect, State Key Lab Biol Plant Dis & Insect Pests, Beijing 100193, Peoples R China

2.Beijing Forestry Univ, Coll Biol Sci & Technol, Natl Engn Lab Tree Breeding, Beijing 100083, Peoples R China

3.Southern Univ Sci & Technol, Sch Life Sci, Inst Plant & Food Sci, Dept Biol, Shenzhen 518055, Guangdong, Peoples R China

4.Beijing Forestry Univ, Beijing Adv Innovat Ctr Tree Breeding Mol Design, Beijing 100083, Peoples R China

关键词： bacterial pathogens; EDS1; jasmonic acid (JA); Pseudomonas syringae pv tomato (Pst) DC3000; salicylic acid (SA); ZAT18

期刊名称：NEW PHYTOLOGIST （ 影响因子：10.323； 五年影响因子：10.768 ）

ISSN： 0028-646X

年卷期： 2022 年 233 卷 3 期

页码：

收录情况： SCI

摘要： Phytopathogens can manipulate plant hormone signaling to counteract immune responses; however, the underlying mechanism is mostly unclear. Here, we report that Pseudomonas syringae pv tomato (Pst) DC3000 induces expression of C2H2 zinc finger transcription factor ZAT18 in a jasmonic acid (JA)-signaling-dependent manner. Biochemical assays further confirmed that ZAT18 is a direct target of MYC2, which is a very important regulator in JA signaling. CRISPR/Cas9-generated zat18-cr mutants exhibited enhanced resistance to Pst DC3000, while overexpression of ZAT18 resulted in impaired disease resistance. Genetic characterization of ZAT18 mutants demonstrated that ZAT18 represses defense responses by inhibiting the accumulation of the key plant immune signaling molecule salicylic acid (SA), which is dependent on its EAR motif. ZAT18 exerted this inhibitory effect by directly repressing the transcription of Enhanced Disease Susceptibility 1 (EDS1), which is the key signaling component of pathogen-induced SA accumulation. Overexpression of ZAT18 resulted in decreased SA content, while loss of function of ZAT18 showed enhanced SA accumulation upon pathogen infection. Furthermore, enhanced resistance and SA content in zat18-cr mutants was abolished by the mutation in EDS1. Our data indicate that pathogens induce ZAT18 expression to repress the transcription of EDS1, further antagonising SA accumulation for bacterial infection.

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