PilG is Involved in the Regulation of Twitching Motility and Antifungal Antibiotic Biosynthesis in the Biological Control Agent Lysobacter enzymogenes
文献类型： 外文期刊
作者： Zhou, Xue 1 ; Qian, Guoliang 1 ; Chen, Yuan 1 ; Du, Liangcheng 3 ; Liu, Fengquan 1 ; Yuen, Gary Y. 5 ;
作者机构： 1.Nanjing Agr Univ, Coll Plant Protect, Nanjing 210095, Jiangsu, Peoples R China
2.Nanjing Agr Univ, Key Lab Integrated Management Crop Dis & Pests, Minist Educ, Nanjing, Jiangsu, Peoples R China
3.Univ Nebraska, Dept Chem, Lincoln, NE 68588 USA
4.Jiangsu Acad Agr Sci, Inst Plant Protect, Nanjing 210014, Jiangsu, Peoples R China
5.Univ Nebraska, Dept Plant Pathol, Lincoln, NE 68583 USA
期刊名称：PHYTOPATHOLOGY （ 影响因子：4.025； 五年影响因子：4.394 ）
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收录情况： SCI
摘要： Lysobacter enzymogenes strain C3 is a gliding bacterium which produces the antifungal secondary metabolite heat-stable antifungal factor (HSAF) and type IV pilus (T4P) as important mechanisms in biological control activity against fungal pathogens. To date, the regulators that control HSAF biosynthesis and T4P-dependent twitching motility in L. enzymogenes are poorly explored. In the present study, we addressed the role of pilG in the regulation of these two traits in L. enzymogenes. PilG of L. enzymogenes was found to be a response regulator, commonly known as a component of a two-component transduction system. Mutation of pilG in strain C3 abolished its ability to display spreading colony phenotype and cell movement at the colony margin, which is indicative of twitching motility; hence, PilG positively regulates twitching motility in L. enzymogenes. Mutation of pilG also enhanced HSAF production and the transcription of its key biosynthetic gene hsaf pks/nrps, suggesting that PilG plays a negative regulatory role in HSAF biosynthesis. This finding represents the first demonstration of the regulator PilG having a role in secondary metabolite biosynthesis in bacteria. Collectively, our results suggest that key ecological functions (HSAF production and twitching motility) in L. enzymogenes strain C3 are regulated in opposite directions by the same regulatory protein, PilG.
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