| pubmed-article:15601868 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:15601868 | lifeskim:mentions | umls-concept:C0332307 | lld:lifeskim |
| pubmed-article:15601868 | lifeskim:mentions | umls-concept:C1167130 | lld:lifeskim |
| pubmed-article:15601868 | lifeskim:mentions | umls-concept:C0031686 | lld:lifeskim |
| pubmed-article:15601868 | lifeskim:mentions | umls-concept:C0076919 | lld:lifeskim |
| pubmed-article:15601868 | lifeskim:mentions | umls-concept:C0040649 | lld:lifeskim |
| pubmed-article:15601868 | lifeskim:mentions | umls-concept:C0086860 | lld:lifeskim |
| pubmed-article:15601868 | lifeskim:mentions | umls-concept:C0205396 | lld:lifeskim |
| pubmed-article:15601868 | lifeskim:mentions | umls-concept:C1704711 | lld:lifeskim |
| pubmed-article:15601868 | lifeskim:mentions | umls-concept:C2587213 | lld:lifeskim |
| pubmed-article:15601868 | pubmed:issue | 1 | lld:pubmed |
| pubmed-article:15601868 | pubmed:dateCreated | 2004-12-16 | lld:pubmed |
| pubmed-article:15601868 | pubmed:abstractText | The Ccr4-Not complex is a conserved global regulator of gene expression, which serves as a regulatory platform that senses and/or transmits nutrient and stress signals to various downstream effectors. Presumed effectors of this complex in yeast are TFIID, a general transcription factor that associates with the core promoter, and Msn2, a key transcription factor that regulates expression of stress-responsive element (STRE)-controlled genes. Here we show that the constitutively high level of STRE-driven expression in ccr4-not mutants results from two independent effects. Accordingly, loss of Ccr4-Not function causes a dramatic Msn2-independent redistribution of TFIID on promoters with a particular bias for STRE-controlled over ribosomal protein gene promoters. In parallel, loss of Ccr4-Not complex function results in an alteration of the posttranslational modification status of Msn2, which depends on the type 1 protein phosphatase Glc7 and its newly identified subunit Bud14. Tests of epistasis as well as transcriptional analyses of Bud14-dependent transcription support a model in which the Ccr4-Not complex prevents activation of Msn2 via inhibition of the Bud14/Glc7 module in exponentially growing cells. Thus, increased activity of STRE genes in ccr4-not mutants may result from both altered general distribution of TFIID and unscheduled activation of Msn2. | lld:pubmed |
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| pubmed-article:15601868 | pubmed:language | eng | lld:pubmed |
| pubmed-article:15601868 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:15601868 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:15601868 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:15601868 | pubmed:month | Jan | lld:pubmed |
| pubmed-article:15601868 | pubmed:issn | 0270-7306 | lld:pubmed |
| pubmed-article:15601868 | pubmed:author | pubmed-author:MailletLauren... | lld:pubmed |
| pubmed-article:15601868 | pubmed:author | pubmed-author:CollartMartin... | lld:pubmed |
| pubmed-article:15601868 | pubmed:author | pubmed-author:WernerMichelM | lld:pubmed |
| pubmed-article:15601868 | pubmed:author | pubmed-author:WinderickxJor... | lld:pubmed |
| pubmed-article:15601868 | pubmed:author | pubmed-author:JamesNicoleN | lld:pubmed |
| pubmed-article:15601868 | pubmed:author | pubmed-author:De... | lld:pubmed |
| pubmed-article:15601868 | pubmed:author | pubmed-author:BisigRuthR | lld:pubmed |
| pubmed-article:15601868 | pubmed:author | pubmed-author:DuboulozFrédé... | lld:pubmed |
| pubmed-article:15601868 | pubmed:author | pubmed-author:PedruzziIvoI | lld:pubmed |
| pubmed-article:15601868 | pubmed:author | pubmed-author:CameroniElisa... | lld:pubmed |
