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

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Lenssen, Eve | James, Nicole | Pedruzzi, Ivo | Dubouloz, †, Frédérique | Cameroni, Elisabetta | Bisig, Ruth | Maillet, Laurent, A | Werner, ‡, Michel | Roosen, Johnny | Petrovic, Katarina | Winderickx, Joris | Collart, Martine, A | de Virgilio, Claudio

Edité par CCSD ; American Society for Microbiology -

International audience. 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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