التفاصيل البيبلوغرافية
| العنوان: |
The Ccr4-Not Complex Independently Controls both Msn2-Dependent Transcriptional Activation—via a Newly Identified G1c7/Bud14 Type... |
| المؤلفون: |
Lenssen, Eve, Nicole James, Ivo Pedruzzi, Frédérique Dubouloz, Elisabetta Cameroni, Ruth Bisig, Laurent Maillet, Michel Werner, Johnny Roosen, Katarina Petrovic, Joris Winderickx, Martine A. Collart, Claudio De Virgilio |
| المصدر: |
Molecular & Cellular Biology; Jan2005, Vol. 25 Issue 1, p488-498, 11p, 2 Diagrams, 7 Charts, 7 Graphs |
| مصطلحات موضوعية: |
PROTEINS, PHOSPHATASES, GENE expression, TRANSCRIPTION factors, RIBOSOMES, CELLS |
| مستخلص: |
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 egectors 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. [ABSTRACT FROM AUTHOR] |
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| قاعدة البيانات: |
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