RpoS-mediated negative control of the Salmonella flagellar regulon

在沙门氏菌属中，鞭毛调节子受固定相特异性σ因子RpoS负调控。本研究旨在阐明这种调控的分子机制.为了鉴定其产物参与这种负调控的基因，使用Tn5诱变分离在RpoS存在下以高水平表达鞭毛基因的去阻遏突变体。保存了一个这样的突变体，其中Tn5插入显示与去阻遏表型100%连锁。Tn5插入位点的序列分析显示，被破坏的基因是nlpC，推测其编码脂蛋白之一。由于该基因不太可能与其他基因构成操纵子，因此我得出结论，NlpC负责鞭毛调节子的RpoS控制。无胸腺嘧啶死亡和鞭毛基因的RpoS控制无胸腺嘧啶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，无胸腺嘧啶死亡被证明是由鞭毛基因的缺陷抑制。由于程序性细胞死亡通常由RpoS调节，因此在鞭毛基因座中搜索RpoS依赖性启动子的DNA序列。发现一个这样的启动子存在于flgJ基因的上游，其编码鞭毛特异性胞壁酶，该酶负责鞭毛形态发生期间肽聚糖层的降解。这一发现表明，在胸腺嘧啶饥饿条件下，RpoS可以增强FlgJ胞壁酶的表达，导致细胞裂解。

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.