Novel insights into the regulatory roles of gene hshB in Xanthomonas oryzae pv. oryzicola
文献类型: 外文期刊
作者: Song, Zhiwei 1 ; Zhao, Yancun 1 ; Qian, Guoliang 2 ; Odhiambo, Benard Omondi 2 ; Liu, Fengquan 1 ;
作者机构: 1.Jiangsu Acad Agr Sci, Inst Plant Protect, Nanjing 210014, Jiangsu, Peoples R China
2.Nanjing Agr Univ, Coll Plant Protect, Nanjing 210095, Jiangsu, Peoples R China
3.Nanjing Agr Univ, Minist Educ, Key Lab Integrated Management Crop Dis & Pests, Nanjing, Jiangsu, Peoples R China
关键词: Xanthomonas oryzae pv. oryzicola;Quorum sensing;hshB;Cell motility;Biofilm formation
期刊名称:RESEARCH IN MICROBIOLOGY ( 影响因子:3.992; 五年影响因子:4.061 )
ISSN:
年卷期:
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收录情况: SCI
摘要: Xanthomonas oryzae pv. oryzicola causes leaf streak disease of rice. The gene hshB is a newly identified virulence-associated gene that is co regulated by diffusible signal factor signaling and global regulator Clp in X. oryzae pv. oryzicola. Our previous study showed that mutation of hshB remarkably impaired the virulence, extracellular protease activity, extracellular polysaccharide production and resistance to oxidative stress of X. oryzae pv. oryzicola. In this study, the regulatory role of hshB in X. oryzae pv.oryzicola was expanded. Results showed that hshB was also required for cell swimming motility. Transcriptome analysis showed that 305 genes were significantly differentially expressed after deletion of hshB in X. oryzae pv. oryzicola. Further analysis of transcriptome data indicated that the differentially expressed genes focused on two aspects: namely, cell motility and cell signal transduction. This finding strongly identified the closely related function of hshB to cell motility and signal transduction. In addition, the mutation of hshB of X. oryzae pv. oryzicola enhanced biofilm formation. Collectively, the study showed novel functions of gene hshB in cell motility and biofilm formation by transcriptome analysis, thus expanding our understanding of the roles of gene hshB in the pathogenic X. oryzae pv. oryzicola. (c) 2016 Institut Pasteur. Published by Elsevier Masson SAS. All rights reserved.
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