Mutations in SIN4 and RGR1 cause constitutive expression of MAL structural genes in Saccharomyces cerevisiae

• Published in: Genetics (Austin) 2004-10, Vol.168 (2), p.747-757
• Main Authors: Wang, X, Michels, C.A
• Format: Article
• Language: English
• Subjects: alpha-Glucosidases - genetics; Binding sites; Chromatin Assembly and Disassembly; Gene expression; Gene Expression Regulation, Fungal; Investigations; Lac Operon; Maltose - metabolism; Mediator Complex; Membrane Transport Proteins - genetics; Monosaccharide Transport Proteins - genetics; Monosaccharide Transport Proteins - metabolism; Mutation; Mutation - genetics; Promoter Regions, Genetic - genetics; Proteins; Repressor Proteins - genetics; Repressor Proteins - metabolism; Saccharomyces cerevisiae; Saccharomyces cerevisiae - genetics; Saccharomyces cerevisiae - metabolism; Saccharomyces cerevisiae Proteins - genetics; Saccharomyces cerevisiae Proteins - metabolism; Symporters - genetics; Symporters - metabolism; Trans-Activators - genetics; Trans-Activators - metabolism; Transcription Factors - genetics; Transcription Factors - metabolism; Yeast
• ISSN: 0016-6731; 1943-2631; 1943-2631
• DOI: 10.1534/genetics.104.029611

Transcription of the Saccharomyces MAL structural genes is induced 40-fold by maltose and requires the MAL-activator and maltose permease. To identify additional players involved in regulating MAL gene expression, we carried out a genetic selection for MAL constitutive mutants. Strain CMY4000 containing MAL1 and integrated copies of MAL61promoter-HIS3 and MAL61promoter-lacZ reporter genes was used to select constitutive mutants. The 29 recessive mutants fall into at least three complementation groups. Group 1 and group 2 mutants exhibit pleiotropic phenotypes and represent alleles of Mediator component genes RGR1 and SIN4, respectively. The rgr1 and sin4 constitutive phenotype does not require either the MAL-activator or maltose permease, indicating that Mediator represses MAL basal expression. Further genetic analysis demonstrates that RGR1 and SIN4 work in a common pathway and each component of the Mediator Sin4 module plays a distinct role in regulating MAL gene expression. Additionally, the Swi/Snf chromatin-remodeling complex is required for full induction, suggesting a role for chromatin remodeling in the regulation of MAL gene expression. A sin4Delta mutation is unable to suppress the defects in MAL gene expression resulting from loss of the Swi/Snf complex component Snf2p. The role of the Mediator in MAL gene regulation is discussed.