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RpoS-mediated negative control of the Salmonella flagellar regulon

RpoS 介导的沙门氏菌鞭毛调节子负控制

基本信息

批准号：
14540567
负责人：
KUTSUKAKE Kazuhiro
金额：
$ 2.3万
依托单位：
OKAYAMA UNIVERSITY
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (C)
财政年份：
2002
资助国家：
日本
起止时间：
2002 至 2003
项目状态：
已结题

来源：
https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-14540567/
关键词：
Salmonella Flagellar regulon Sigma factor Transcriptional regulation Stationary phase Thymine starvation Programmed cell death Cell lysis 抑圧突然変異トランスポゾンリポプロテイン

项目摘要

In Salmonella, the flagellar regulon is regulated negatively by RpoS, the stationary phase-specific sigma factor. This study was carried out to elucidate the molecular mechanism of this regulation.1. Suppressor analysisIn order to identify a gene whose product is involved in this negative regulation, derepression mutants expressing the flagellar genes at a high level in the presence of RpoS were isolated using Tn5 mutagenesis. One such mutant was saved, in which the Tn5 insertion showed a 100% linkage with the derepression phenotype. Sequence analysis of the Tn5 insertion site revealed that the disrupted gene is nlpC, which is presumed to encode one of the lipoproteins. Because this gene is unlikely to constitute an operon with any other genes, I conclude that NlpC is responsible for RpoS control of the flagellar regulon.2. Thymineless death and RpoS control of flagellar geneThymineless,death is one of the phenomena known as the programmed cell death in bacteria. In this study, thymineless death was shown to be suppressed by defects in flagellar genes. Because programmed cell death is often regulated by RpoS, a RpoS-dependent promoter was searched for DNA sequences in the flagellar loci. One such promoter was found to exist upstream of the flgJ gene, which encodes a flagellum-specific muramidase responsible for degradation of the peptidoglycan layer during flagellar morphogenesis. This finding suggests that in the thymine starvation condition RpoS may enhance the expression of the FlgJ muramidase resulting in cell lysis.

在沙门氏菌中，鞭毛调节子受到rpos的负调控，rpos是一种固定相特异的sigma因子。本研究旨在阐明这一调控的分子机制。抑制子分析为了确定其产物参与这一负调控的基因，利用Tn5诱变技术分离了在rpos存在下高水平表达鞭毛基因的去抑制突变体。保存了一个这样的突变体，其中Tn5插入与去阻遏表型100%连锁。对Tn5插入位点的序列分析表明，被破坏的基因是NLPC，推测它编码其中一种脂蛋白。因为这个基因不太可能与任何其他基因构成操纵子，所以我得出结论，NLPC负责鞭毛调节的rpos控制。无胸腺细胞死亡和rpos控制鞭毛无胸腺基因，死亡是细菌中被称为程序性细胞死亡的现象之一。在这项研究中，鞭毛基因的缺陷抑制了无胸腺嘧啶的死亡。由于细胞程序性死亡通常由rpos调控，因此在鞭毛基因座上搜索rpos依赖的启动子以寻找DNA序列。一个这样的启动子被发现存在于flgJ基因的上游，该基因编码一种鞭毛特异性的溶菌胺酶，负责在鞭毛形态发生过程中降解肽聚糖层。这一发现表明，在胸腺嘧啶饥饿的条件下，rpos可能会增强FlgJ溶菌酶的表达，从而导致细胞溶解。