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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

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 post-translational 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.
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https://www.hal.inserm.fr/inserm-02448589
Contributor : Laurent Maillet <>
Submitted on : Wednesday, January 22, 2020 - 1:30:18 PM
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Eve Lenssen, Nicole James, Ivo Pedruzzi, † Dubouloz, Elisabetta Cameroni, et al.. 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. Molecular and Cellular Biology, American Society for Microbiology, 2005, 25, pp.488 - 498. ⟨10.1128/MCB.25.1.488-498.2005⟩. ⟨inserm-02448589⟩

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