acid-induced type vi secretion system is regulated by exor-chvgchvi signaling cascade in agrobacterium tumefaciens第六段型分泌系统是由根癌土壤杆菌exor-chvgchvi信号级联.pdfVIP

acid-induced type vi secretion system is regulated by exor-chvgchvi signaling cascade in agrobacterium tumefaciens第六段型分泌系统是由根癌土壤杆菌exor-chvgchvi信号级联.pdf

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acid-induced type vi secretion system is regulated by exor-chvgchvi signaling cascade in agrobacterium tumefaciens第六段型分泌系统是由根癌土壤杆菌exor-chvgchvi信号级联

Acid-Induced Type VI Secretion System Is Regulated by ExoR-ChvG/ChvI Signaling Cascade in Agrobacterium tumefaciens 1,2. 1. 2 1 Chih-Feng Wu , Jer-Sheng Lin , Gwo-Chyuan Shaw *, Erh-Min Lai * 1 Institute of Plant and Microbial Biology, Academia Sinica, Taipei, Taiwan, 2 Institute of Biochemistry and Molecular Biology, National Yang-Ming University, Taipei, Taiwan Abstract The type VI secretion system (T6SS) is a widespread, versatile protein secretion system in pathogenic Proteobacteria. Several T6SSs are tightly regulated by various regulatory systems at multiple levels. However, the signals and/or regulatory mechanisms of many T6SSs remain unexplored. Here, we report on an acid-induced regulatory mechanism activating T6SS in Agrobacterium tumefaciens, a plant pathogenic bacterium causing crown gall disease in a wide range of plants. We monitored the secretion of the T6SS hallmark protein hemolysin-coregulated protein (Hcp) from A. tumefaciens and found that acidity is a T6SS-inducible signal. Expression analysis of the T6SS gene cluster comprising the imp and hcp operons revealed that imp expression and Hcp secretion are barely detected in A. tumefaciens grown in neutral minimal medium but are highly induced with acidic medium. Loss- and gain-of-function analysis revealed that the A. tumefaciens T6SS is positively regulated by a chvG/chvI two-component system and negatively regulated by exoR. Further epistasis analysis revealed that exoR functions upstream of the chvG sensor kinase in regulating T6SS. ChvG protein levels are greatly increased in the exoR deletion mutant and the periplasmic form of overexpressed ExoR is rapidly degraded under acidic

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