pubmed-article:1592811 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:1592811 | lifeskim:mentions | umls-concept:C1336789 | lld:lifeskim |
pubmed-article:1592811 | lifeskim:mentions | umls-concept:C0815304 | lld:lifeskim |
pubmed-article:1592811 | lifeskim:mentions | umls-concept:C1511938 | lld:lifeskim |
pubmed-article:1592811 | pubmed:issue | 11 | lld:pubmed |
pubmed-article:1592811 | pubmed:dateCreated | 1992-7-1 | lld:pubmed |
pubmed-article:1592811 | pubmed:abstractText | Sin is a Bacillus subtilis DNA-binding protein which is essential for competence, motility, and autolysin production but also, if expressed on a multicopy plasmid, is inhibitory to sporulation and alkaline protease synthesis. We have now examined the physiological role of Sin in sporulation and found that this protein specifically represses three stage II sporulation genes (spoIIA, spoIIE, and spoIIG) but not the earlier-acting stage 0 sporulation genes. sin loss-of-function mutations cause higher expression of stage II genes and result in a higher frequency of sporulation, in general. Sin binds to the upstream promoter region of spoIIA in vitro and may thus gate entry into sporulation by directly repressing the transcription of stage II genes. In vivo levels of Sin increase rather than decrease at the time of stage II gene induction, suggesting that posttranslational modification may play a role in downregulation of negative Sin function. | lld:pubmed |
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pubmed-article:1592811 | pubmed:language | eng | lld:pubmed |
pubmed-article:1592811 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:1592811 | pubmed:citationSubset | IM | lld:pubmed |
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pubmed-article:1592811 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:1592811 | pubmed:month | Jun | lld:pubmed |
pubmed-article:1592811 | pubmed:issn | 0021-9193 | lld:pubmed |
pubmed-article:1592811 | pubmed:author | pubmed-author:SmithII | lld:pubmed |
pubmed-article:1592811 | pubmed:author | pubmed-author:GaurNN | lld:pubmed |
pubmed-article:1592811 | pubmed:author | pubmed-author:BayEE | lld:pubmed |
pubmed-article:1592811 | pubmed:author | pubmed-author:Mandic-MulecI... | lld:pubmed |
pubmed-article:1592811 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:1592811 | pubmed:volume | 174 | lld:pubmed |
pubmed-article:1592811 | pubmed:geneSymbol | spoIIE | lld:pubmed |
pubmed-article:1592811 | pubmed:geneSymbol | spoIIA | lld:pubmed |
pubmed-article:1592811 | pubmed:geneSymbol | spoIIG | lld:pubmed |
pubmed-article:1592811 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:1592811 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:1592811 | pubmed:pagination | 3561-9 | lld:pubmed |
pubmed-article:1592811 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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pubmed-article:1592811 | pubmed:year | 1992 | lld:pubmed |
pubmed-article:1592811 | pubmed:articleTitle | Sin, a stage-specific repressor of cellular differentiation. | lld:pubmed |
pubmed-article:1592811 | pubmed:affiliation | Department of Microbiology, New York University School of Medicine, New York 10016. | lld:pubmed |
pubmed-article:1592811 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:1592811 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
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