An Arabidopsis Secondary Metabolite Directly Targets Expression of the Bacterial Type III Secretion System to Inhibit Bacterial Virulence

Plants deploy a variety of secondary metabolites to fend off pathogen attack. Although defense compounds are generally considered toxic to microbes, the exact mechanisms are often unknown. Here, we show that the Arabidopsis defense compound sulforaphane (SFN) functions primarily by inhibiting Pseudo...

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Published in:Cell host & microbe Vol. 27; no. 4; p. 601
Main Authors: Wang, Wei, Yang, Jing, Zhang, Jian, Liu, Yong-Xin, Tian, Caiping, Qu, Baoyuan, Gao, Chulei, Xin, Peiyong, Cheng, Shujing, Zhang, Wenjing, Miao, Pei, Li, Lei, Zhang, Xiaojuan, Chu, Jinfang, Zuo, Jianru, Li, Jiayang, Bai, Yang, Lei, Xiaoguang, Zhou, Jian-Min
Format: Journal Article
Language:English
Published: United States 08.04.2020
Subjects:
Arabidopsis - metabolism
Bacterial Proteins - drug effects
Cysteine - drug effects
Cysteine - metabolism
Disease Resistance
Gene Expression Regulation, Bacterial
Isothiocyanates - metabolism
Isothiocyanates - pharmacology
Plant Diseases - microbiology
Pseudomonas syringae - drug effects
Pseudomonas syringae - metabolism
Secondary Metabolism
Transcription Factors - drug effects
Type III Secretion Systems - drug effects
Type III Secretion Systems - genetics
defense compound
glucosinolate
Arabidopsis
Pseudomonas syringae
Type III Secretion System
ISSN:1934-6069, 1934-6069
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Summary:Plants deploy a variety of secondary metabolites to fend off pathogen attack. Although defense compounds are generally considered toxic to microbes, the exact mechanisms are often unknown. Here, we show that the Arabidopsis defense compound sulforaphane (SFN) functions primarily by inhibiting Pseudomonas syringae type III secretion system (TTSS) genes, which are essential for pathogenesis. Plants lacking the aliphatic glucosinolate pathway, which do not accumulate SFN, were unable to attenuate TTSS gene expression and exhibited increased susceptibility to P. syringae strains that cannot detoxify SFN. Chemoproteomics analyses showed that SFN covalently modified the cysteine at position 209 of HrpS, a key transcription factor controlling TTSS gene expression. Site-directed mutagenesis and functional analyses further confirmed that Cys209 was responsible for bacterial sensitivity to SFN in vitro and sensitivity to plant defenses conferred by the aliphatic glucosinolate pathway. Collectively, these results illustrate a previously unknown mechanism by which plants disarm a pathogenic bacterium.
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ISSN:1934-6069
1934-6069
DOI:10.1016/j.chom.2020.03.004