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OmpR负向调节小肠结肠炎耶尔森菌中侵袭素的表达。

OmpR negatively regulates expression of invasin in Yersinia enterocolitica.

作者信息

Brzostek Katarzyna, Brzóstkowska Marta, Bukowska Iwona, Karwicka Ewa, Raczkowska Adrianna

机构信息

Department of Applied Microbiology, Institute of Microbiology, Warsaw University, Miecznikowa 1, 02-096 Warsaw, Poland.

出版信息

Microbiology (Reading). 2007 Aug;153(Pt 8):2416-2425. doi: 10.1099/mic.0.2006/003202-0.

Abstract

Invasin, the major adhesion and invasion factor of Yersinia enterocolitica, is encoded by the inv gene, which is regulated by growth phase and in response to a variety of environmental conditions such as temperature, pH and osmolarity. So far, three proteins, RovA, H-NS and YmoA, have been identified as factors regulating the expression of the inv gene in enteropathogenic Yersinia. Here, data from inv' : : lacZYA chromosomal gene fusion studies are presented indicating that OmpR, the response regulator of the EnvZ/OmpR two-component system, acts to negatively regulate inv expression at the transcriptional level at 25 degrees C, and that high osmolarity enhances the inhibitory effect of this protein. In a strain lacking OmpR the expression of inv at 25 degrees C was increased sixfold, but at 37 degrees C, a temperature known to repress inv expression, this effect was not observed, suggesting that temperature regulation of inv is OmpR-independent. Furthermore, the expression of inv in the ompR background was no longer responsive to increased osmolarity. Complementation with the active ompR allele restored wild-type inv expression in the ompR mutant. In silico analysis of the Y. enterocolitica O : 9 inv promoter sequence revealed the presence of an OmpR consensus binding site located in the -15 to -33 region. OmpR was able to specifically bind to a fragment of the inv promoter containing this putative binding site in electrophoretic mobility shift assays. Thus, OmpR seems to be a repressor of inv in Y. enterocolitica.

摘要

侵袭素是小肠结肠炎耶尔森菌的主要黏附与侵袭因子,由inv基因编码,该基因受生长阶段调控,并对多种环境条件作出反应,如温度、pH值和渗透压。到目前为止,已鉴定出三种蛋白质,即RovA、H-NS和YmoA,它们是调节致病性耶尔森菌中inv基因表达的因子。在此,我们展示了来自inv'::lacZYA染色体基因融合研究的数据,表明EnvZ/OmpR双组分系统的反应调节因子OmpR在25℃时在转录水平上对inv表达起负调控作用,并且高渗透压增强了该蛋白的抑制作用。在缺乏OmpR的菌株中,inv在25℃时的表达增加了6倍,但在37℃(已知该温度会抑制inv表达)时未观察到这种效应,这表明inv的温度调节不依赖于OmpR。此外,在ompR背景下inv的表达不再对渗透压升高作出反应。用活性ompR等位基因进行互补可恢复ompR突变体中的野生型inv表达。对小肠结肠炎耶尔森菌O:9 inv启动子序列的计算机分析揭示,在-15至-33区域存在一个OmpR共有结合位点。在电泳迁移率变动分析中,OmpR能够特异性结合包含该假定结合位点的inv启动子片段。因此,OmpR似乎是小肠结肠炎耶尔森菌中inv的一个阻遏物。

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