RpoS-mediated negative control of the Salmonella flagellar regulon
| Project/Area Number |
14540567
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
遺伝
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| Research Institution | OKAYAMA UNIVERSITY |
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Principal Investigator |
KUTSUKAKE Kazuhiro OKAYAMA UNIVERSITY, Faculty of Science, Professor, 理学部, 教授 (90143362)
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| Co-Investigator(Kenkyū-buntansha) |
IYODA Sunao National Institute of Infectious Disease, Microbiology Division, Chief investigator, 細菌第一部, 主任研究員 (70300928)
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| Project Period (FY) |
2002 – 2003
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| Project Status |
Completed (Fiscal Year 2003)
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| Budget Amount *help |
¥3,600,000 (Direct Cost: ¥3,600,000)
Fiscal Year 2003: ¥1,800,000 (Direct Cost: ¥1,800,000)
Fiscal Year 2002: ¥1,800,000 (Direct Cost: ¥1,800,000)
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| Keywords | 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 |
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| Research Abstract |
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 analysis
In 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 gene
Thymineless,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.
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Report
(3 results)
Research Products
(18 results)
