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Regulation of the Edwardsiella tarda Hemolysin Gene and luxS by EthR

文献类型: 外文期刊

作者: Wang Fang 1 ; Zhang, Min 1 ; Hu, Yong-hua 1 ; Zhang, Wei-wei 1 ; Sun, Li 1 ;

作者机构: 1.Chinese Acad Sci, Inst Oceanol, Qingdao 266071, Peoples R China

2.Chinese Acad Sci, Grad Univ, Beijing 100049, Peoples R China

3.Chinese Acad Fishery Sci, Yellow Sea Fisheries Res Inst, Qingdao 266071, Peoples R China

关键词: Edwardsiella tarda;hemolysin;luxS;RNAi;virulence

期刊名称:JOURNAL OF MICROBIOLOGY AND BIOTECHNOLOGY ( 影响因子:2.351; 五年影响因子:2.65 )

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收录情况: SCI

摘要: Edwardsiella tarda is a pathogen with a broad host range that includes human and animals. The E. tarda hemolysin (Eth) system, which comprises EthA and EthB, is a noted virulence element that is widely distributed in pathogenic isolates of E. tarda. Previous study has shown that the expression of ethB is regulated by iron, which suggests the possibility that the ferric uptake regulator (Fur) is involved in the regulation of ethB. The work presented in this report supports the previous findings and demonstrates that ethB expression was decreased under conditions when the E. tarda Fur (Fur(Et)) was overproduced, and enhanced when Fur(Et) was inactivated. We also identified a second ethB regulator, EthR, which is a transcription regulator of the GntR family. EthR represses ethB expression by direct interaction with the ethB promoter region. In addition to ethB, EthR also modulates, but positively, luxS expression and AI-2 production by binding to the luxS promoter region. The expression of ethR itself is subject to negative autoregulation; interference with this regulation by overexpressing ethR during the process of infection caused (i) drastic changes in ethB and luxS expressions, (ii) vitiation in the tissue dissemination and survival ability of the bacterium, and (iii) significant attenuation of the overall bacterial virulence. These results not only provide new insights into the regulation mechanisms of the Eth hemolysin and LuxS/AI-2 quorum sensing systems but also highlight the importance of these systems in bacterial virulence.

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