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致病性迟缓爱德华氏菌菌株fur(铁摄取调节蛋白)基因的分子分析

Molecular analysis of the fur (ferric uptake regulator) gene of a pathogenic Edwardsiella tarda strain.

作者信息

Wang Fang, Cheng Shuang, Sun Kun, Sun Li

机构信息

Institute of Oceanology, Chinese Academy of Sciences, Qingdao, PR China.

出版信息

J Microbiol. 2008 Jun;46(3):350-5. doi: 10.1007/s12275-008-0038-x. Epub 2008 Jul 5.

Abstract

The gene encoding the Edwardsiella tarda ferric uptake regulator (Fur(Et)) was cloned from a pathogenic E. tarda strain isolated from diseased fish. Fur(Et) shares 90% overall sequence identity with the Escherichia coli Fur (Fur(Ec)) and was able to complement the mutant phenotype of a fur (Ec)-defective E. coli strain. Mutational analysis indicated that C92S and C95S mutations inactivated Fur(Et) whereas E112K mutation resulted in a superactive Fur(Et) variant. Fur(Et) negatively regulated its own expression; interruption of this regulation impaired bacterial growth, altered the production of certain outer membrane proteins, and attenuated bacterial virulence.

摘要

从患病鱼分离出的致病性迟缓爱德华氏菌菌株中克隆出编码迟缓爱德华氏菌铁摄取调节蛋白(Fur(Et))的基因。Fur(Et)与大肠杆菌铁摄取调节蛋白(Fur(Ec))的整体序列同一性为90%,并且能够互补fur(Ec)缺陷型大肠杆菌菌株的突变表型。突变分析表明,C92S和C95S突变使Fur(Et)失活,而E112K突变导致Fur(Et)变体超活性。Fur(Et)对其自身表达起负调控作用;这种调控的中断损害细菌生长,改变某些外膜蛋白的产生,并减弱细菌毒力。

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