State Key Laboratory of Plant Genomics, Institute of Genetics and Developmental Biology, Innovation Academy for Seed Design, Chinese Academy of Sciences, Beijing 100101, China; CAS Center for Excellence in Biotic Interactions, University of Chinese Academy of Sciences, Beijing 100049, China.
State Key Laboratory of Proteomics, Beijing Proteome Research Center, National Center for Protein Sciences Beijing, Beijing Institute of Lifeomics, Beijing 102206, China.
Cell Host Microbe. 2020 Apr 8;27(4):601-613.e7. doi: 10.1016/j.chom.2020.03.004.
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.
植物会产生多种次生代谢物来抵御病原体的攻击。虽然防御化合物通常被认为对微生物有毒，但确切的机制往往未知。在这里，我们表明拟南芥防御化合物萝卜硫素（SFN）主要通过抑制丁香假单胞菌 III 型分泌系统（TTSS）基因起作用，该基因对致病至关重要。缺乏脂肪族芥子油苷途径的植物不会积累 SFN，因此无法减弱 TTSS 基因的表达，并且对无法解毒 SFN 的丁香假单胞菌菌株的敏感性增加。化学蛋白质组学分析表明，SFN 与 HrpS 第 209 位半胱氨酸发生了共价修饰，HrpS 是控制 TTSS 基因表达的关键转录因子。定点突变和功能分析进一步证实，Cys209 负责细菌对 SFN 的体外敏感性以及脂肪族芥子油苷途径赋予植物防御的敏感性。总的来说，这些结果说明了植物使致病细菌失去能力的一种先前未知的机制。
