| pubmed-article:14671322 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:14671322 | lifeskim:mentions | umls-concept:C0035820 | lld:lifeskim |
| pubmed-article:14671322 | lifeskim:mentions | umls-concept:C0038952 | lld:lifeskim |
| pubmed-article:14671322 | lifeskim:mentions | umls-concept:C0017262 | lld:lifeskim |
| pubmed-article:14671322 | lifeskim:mentions | umls-concept:C2611014 | lld:lifeskim |
| pubmed-article:14671322 | lifeskim:mentions | umls-concept:C0851285 | lld:lifeskim |
| pubmed-article:14671322 | lifeskim:mentions | umls-concept:C0439799 | lld:lifeskim |
| pubmed-article:14671322 | lifeskim:mentions | umls-concept:C2348532 | lld:lifeskim |
| pubmed-article:14671322 | lifeskim:mentions | umls-concept:C2911684 | lld:lifeskim |
| pubmed-article:14671322 | lifeskim:mentions | umls-concept:C0185117 | lld:lifeskim |
| pubmed-article:14671322 | pubmed:issue | 26 | lld:pubmed |
| pubmed-article:14671322 | pubmed:dateCreated | 2003-12-24 | lld:pubmed |
| pubmed-article:14671322 | pubmed:abstractText | The mechanosensitive (MS) channels MscS and MscL are essential for the survival of hypoosmotic shock by Escherichia coli cells. We demonstrate that MscS and MscL are induced by osmotic stress and by entry into stationary phase. Reduced levels of MS proteins and reduced expression of mscL- and mscS-LacZ fusions in an rpoS mutant strain suggested that the RNA polymerase holoenzyme containing sigmaS is responsible, at least in part, for regulating production of MS channel proteins. Consistent with the model that the effect of sigmaS is direct, the MscS and MscL promoters both use RNA polymerase containing sigmaS in vitro. Conversely, clpP or rssB mutations, which cause enhanced levels of sigmaS, show increased MS channel protein synthesis. RpoS null mutants are sensitive to hypoosmotic shock upon entry into stationary phase. These data suggest that MscS and MscL are components of the RpoS regulon and play an important role in ensuring structural integrity in stationary phase bacteria. | lld:pubmed |
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| pubmed-article:14671322 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:14671322 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:14671322 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:14671322 | pubmed:month | Dec | lld:pubmed |
| pubmed-article:14671322 | pubmed:issn | 0027-8424 | lld:pubmed |
| pubmed-article:14671322 | pubmed:author | pubmed-author:GourseRichard... | lld:pubmed |
| pubmed-article:14671322 | pubmed:author | pubmed-author:BoothIan RIR | lld:pubmed |
| pubmed-article:14671322 | pubmed:author | pubmed-author:MillerSamanth... | lld:pubmed |
| pubmed-article:14671322 | pubmed:author | pubmed-author:MurrayHeath... | lld:pubmed |
| pubmed-article:14671322 | pubmed:author | pubmed-author:BartlettWendy... | lld:pubmed |
| pubmed-article:14671322 | pubmed:author | pubmed-author:HOCKADAYT DTD | lld:pubmed |
| pubmed-article:14671322 | pubmed:author | pubmed-author:StokesNeil... | lld:pubmed |
| pubmed-article:14671322 | pubmed:author | pubmed-author:SubramaniamCh... | lld:pubmed |
| pubmed-article:14671322 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:14671322 | pubmed:day | 23 | lld:pubmed |
| pubmed-article:14671322 | pubmed:volume | 100 | lld:pubmed |
| pubmed-article:14671322 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:14671322 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:14671322 | pubmed:pagination | 15959-64 | lld:pubmed |
| pubmed-article:14671322 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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| pubmed-article:14671322 | pubmed:year | 2003 | lld:pubmed |
