pubmed-article:18191220 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:18191220 | lifeskim:mentions | umls-concept:C0085454 | lld:lifeskim |
pubmed-article:18191220 | lifeskim:mentions | umls-concept:C0162638 | lld:lifeskim |
pubmed-article:18191220 | lifeskim:mentions | umls-concept:C0035696 | lld:lifeskim |
pubmed-article:18191220 | lifeskim:mentions | umls-concept:C1527148 | lld:lifeskim |
pubmed-article:18191220 | lifeskim:mentions | umls-concept:C0086597 | lld:lifeskim |
pubmed-article:18191220 | pubmed:issue | 1 | lld:pubmed |
pubmed-article:18191220 | pubmed:dateCreated | 2008-1-14 | lld:pubmed |
pubmed-article:18191220 | pubmed:abstractText | In prokaryotes, the toxin-antitoxin systems are thought to play important roles in growth regulation under stress conditions. In the E. coli MazE-MazF system, MazF toxin functions as an mRNA interferase cleaving mRNAs at ACA sequences to inhibit protein synthesis leading to cell growth arrest. Myxococcus xanthus is a bacterium displaying multicellular fruiting body development during which approximately 80% of cells undergo obligatory cell lysis. Here, we demonstrate that M. xanthus has a solitary mazF gene that lacks a cotranscribed antitoxin gene. The mazF deletion results in elimination of the obligatory cell death during development causing dramatic reduction in spore formation. Surprisingly, MrpC, a key developmental regulator, functions as a MazF antitoxin and a mazF transcription activator. Transcription of mrpC and mazF is negatively regulated via MrpC phosphorylation by a Ser/Thr kinase cascade. These findings reveal the regulated deployment of a toxin gene for developmental programmed cell death in bacteria. | lld:pubmed |
pubmed-article:18191220 | pubmed:language | eng | lld:pubmed |
pubmed-article:18191220 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:18191220 | pubmed:citationSubset | IM | lld:pubmed |
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pubmed-article:18191220 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:18191220 | pubmed:month | Jan | lld:pubmed |
pubmed-article:18191220 | pubmed:issn | 0092-8674 | lld:pubmed |
pubmed-article:18191220 | pubmed:author | pubmed-author:InouyeMasayor... | lld:pubmed |
pubmed-article:18191220 | pubmed:author | pubmed-author:NariyaHirofum... | lld:pubmed |
pubmed-article:18191220 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:18191220 | pubmed:day | 11 | lld:pubmed |
pubmed-article:18191220 | pubmed:volume | 132 | lld:pubmed |
pubmed-article:18191220 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:18191220 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:18191220 | pubmed:pagination | 55-66 | lld:pubmed |
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pubmed-article:18191220 | pubmed:year | 2008 | lld:pubmed |
pubmed-article:18191220 | pubmed:articleTitle | MazF, an mRNA interferase, mediates programmed cell death during multicellular Myxococcus development. | lld:pubmed |
pubmed-article:18191220 | pubmed:affiliation | Department of Biochemistry, Robert Wood Johnson Medical School, Piscataway, NJ 08854, USA. | lld:pubmed |
pubmed-article:18191220 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:18191220 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
entrez-gene:947252 | entrezgene:pubmed | pubmed-article:18191220 | lld:entrezgene |
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