PMID:15601868

Citation	Lenssen, E, James, N, Pedruzzi, I, Dubouloz, F, Cameroni, E, Bisig, R, Maillet, L, Werner, M, Roosen, J, Petrovic, K, Winderickx, J, Collart, MA and De Virgilio, C (2005) The Ccr4-Not complex independently controls both Msn2-dependent transcriptional activation--via a newly identified Glc7/Bud14 type I protein phosphatase module--and TFIID promoter distribution. Mol. Cell. Biol. 25:488-98
Abstract	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.
Links	PubMed PMC538800 Online version:10.1128/MCB.25.1.488-498.2005
Keywords	Cell Cycle Proteins/physiology; Cross-Linking Reagents/pharmacology; DNA/metabolism; DNA-Binding Proteins/physiology; Gene Expression Regulation; Genotype; Glucose/metabolism; Immunoblotting; Immunoprecipitation; Models, Biological; Mutation; Nucleic Acid Hybridization; Phosphoprotein Phosphatases/metabolism; Plasmids/metabolism; Promoter Regions, Genetic; Protein Binding; Protein Phosphatase 1; Protein Processing, Post-Translational; RNA, Messenger/metabolism; Ribonucleases/physiology; Saccharomyces cerevisiae/metabolism; Saccharomyces cerevisiae Proteins/metabolism; Saccharomyces cerevisiae Proteins/physiology; Time Factors; Transcription Factor TFIID/chemistry; Transcription Factors/physiology; Transcription, Genetic; Transcriptional Activation; Two-Hybrid System Techniques
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