Tomoyasu Toshifumi, Takaya Akiko, Handa Yutaka, Karata Kiyonobu, Yamamoto Tomoko
Department of Microbiology and Molecular Genetics, Graduate School of Pharmaceutical Sciences, Chiba University, Chiba 263-8522, Japan.
FEMS Microbiol Lett. 2005 Dec 1;253(1):59-66. doi: 10.1016/j.femsle.2005.09.020. Epub 2005 Sep 23.
Enterohaemorrhagic Escherichia coli (EHEC) contains a 36-kb pathogenicity island termed the locus of enterocyte effacement (LEE), which encodes a type III secretion system (TTSS) and virulence proteins. In this paper, we show that the O157:H7 Sakai clpPX mutant strongly impaired the secretion of virulence proteins by TTSS and repressed transcription from all the LEE promoters. The rpoS mutation in O157:H7 Sakai enhanced the transcription from all the LEE promoters and the secretion of virulence proteins, and it could partially suppress the defects of the clpPX mutation. These data indicate that the O157:H7 Sakai ClpXP protease is a positive regulator for LEE expression and that this regulation occurs by two pathways: the sigma(S)-dependent and -independent pathways.
肠出血性大肠杆菌（EHEC）含有一个36千碱基对的致病岛，称为肠上皮细胞损伤位点（LEE），它编码III型分泌系统（TTSS）和毒力蛋白。在本文中，我们表明O157:H7阪崎株的clpPX突变体严重损害了TTSS对毒力蛋白的分泌，并抑制了所有LEE启动子的转录。O157:H7阪崎株的rpoS突变增强了所有LEE启动子的转录和毒力蛋白的分泌，并且它可以部分抑制clpPX突变的缺陷。这些数据表明，O157:H7阪崎株的ClpXP蛋白酶是LEE表达的正调控因子，并且这种调控通过两条途径发生：依赖于σ(S)的途径和不依赖于σ(S)的途径。
