Analysis of URSg-mediated glucose repression of the GAL1 promoter of Saccharomyces cerevisiae

• Published in: Genetics (Austin) 1992-02, Vol.130 (2), p.295-304
• Main Authors: FLICK, J. S, JOHNSTON, M
• Format: Article
• Language: English
• Subjects: adn; Base Sequence; Biological and medical sciences; dna; DNA, Fungal - genetics; expresion genica; expression des genes; Fundamental and applied biological sciences. Psychology; gene; gene expression; genes; Genes, Fungal; Genes, Regulator; Genetic Complementation Test; Genetic Linkage; genetica; genetics; genetique; glucosa; glucose; Glucose - pharmacology; induced mutation; inhibicion; inhibition; Molecular and cellular biology; Molecular genetics; Molecular Sequence Data; mutacion inducida; mutant; mutantes; mutants; Mutation; mutation provoquee; Promoter Regions, Genetic - drug effects; proteinas; proteine; proteins; saccharomyces cerevisiae; Saccharomyces cerevisiae - drug effects; Saccharomyces cerevisiae - genetics; Transcription, Genetic; Transcription. Transcription factor. Splicing. Rna processing
• ISSN: 0016-6731; 1943-2631; 1943-2631
• DOI: 10.1093/genetics/130.2.295

Repression of GAL1 expression during growth on glucose is mediated in part by cis-acting promoter elements designated URS(G) We show that oligonucleotides containing sequences from two regions of URS(G) confer glucose repression upon a heterologous promoter. Repression caused by URS(G) is dependent on trans-acting factors of the glucose repression pathway and is independent of orientation or location within a promoter, suggesting that URS(G) contains binding sites for a glucose-activated repressor protein(s). Genetic analysis identified three apparently novel genes (URR1, URR3 and URR4) that are specifically required for URS(G)-mediated repression and may encode such repressor proteins. Mutations in the URR genes suppress the defect in URS(G), derepression caused by a snf1 mutation.