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The Snf1 kinase controls glucose repression in yeast by modulating interactions between the Mig1 repressor and the Cyc8‐Tup1 co‐repressor
Author(s) -
PapamichosChronakis Manolis,
Gligoris Thomas,
Tzamarias Dimitris
Publication year - 2004
Publication title -
embo reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.584
H-Index - 184
eISSN - 1469-3178
pISSN - 1469-221X
DOI - 10.1038/sj.embor.7400120
Subject(s) - psychological repression , repressor , microbiology and biotechnology , phosphorylation , transcription factor , biology , chemistry , biochemistry , gene expression , gene
Among lower eukaryotes, glucose repression is a conserved, widely spread mechanism regulating carbon catabolism. The yeast Snf1 kinase, the Mig1 DNA‐binding repressor and the Mig1‐interacting co‐repressor complex Cyc8(Ssn6)–Tup1 are central components of this pathway. Previous experiments suggested that cytoplasmic translocation of Mig1, upon its phosphorylation by Snf1 in the nucleus, is the key regulatory step for releasing glucose repression. In this report we re‐evaluate this model. We establish the coordinated repressive action of Mig1 and Cyc8–Tup1 on GAL1 transcription, but we find that Cyc8–Tup1 is not tethered by Mig1 to the promoter DNA. We demonstrate that both negative regulators occupy GAL1 continuously under either repression or activation conditions, although the majority of the Mig1 is redistributed to the cytoplasm upon activation. We show that Snf1‐dependent phosphorylation of Mig1 abolishes interaction with Cyc8–Tup1, and we propose that regulation of this interaction, not the Mig1 cytoplasmic localization, is the molecular switch that controls transcriptional repression/de‐repression.