The Transcriptional Coactivators SAGA, SWI/SNF, and Mediator Make Distinct Contributions to Activation of Glucose-repressed Genes

• Published in: The Journal of biological chemistry Vol. 283; no. 48; pp. 33101 - 33109
• Main Authors: Biddick, Rhiannon K., Law, G. Lynn, Chin, Kevin Khaw Beng, Young, Elton T.
• Format: Journal Article
• Language: English
• Published: United States Elsevier Inc 28-11-2008; American Society for Biochemistry and Molecular Biology
• Subjects: Alcohol Dehydrogenase - genetics; Alcohol Dehydrogenase - metabolism; Chromatin - genetics; Chromatin - metabolism; Chromatin Assembly and Disassembly - physiology; Chromosomal Proteins, Non-Histone - genetics; Chromosomal Proteins, Non-Histone - metabolism; Fructose-Bisphosphatase; Gene Expression Regulation, Fungal - physiology; Glucose - genetics; Glucose - metabolism; Response Elements - physiology; Saccharomyces cerevisiae - genetics; Saccharomyces cerevisiae - metabolism; Saccharomyces cerevisiae Proteins - genetics; Saccharomyces cerevisiae Proteins - metabolism; Trans-Activators - genetics; Trans-Activators - metabolism
• ISSN: 0021-9258; 1083-351X
• DOI: 10.1074/jbc.M805258200

The paradigm of activation via ordered recruitment has evolved into a complicated picture as the influence of coactivators and chromatin structures on gene regulation becomes understood. We present here a comprehensive study of many elements of activation of ADH2 and FBP1, two glucose-regulated genes. We identify SWI/SNF as the major chromatin-remodeling complex at these genes, whereas SAGA (Spt-Ada-Gcn5-acetyltransferase complex) is required for stable recruitment of other coactivators. Mediator plays a crucial role in expression of both genes but does not affect chromatin remodeling. We found that Adr1 bound unaided by coactivators to ADH2, but Cat8 binding depended on coactivators at FBP1. Taken together, our results suggest that commonly regulated genes share many aspects of activation, but that gene-specific regulators or elements of promoter architecture may account for small differences in the mechanism of activation. Finally, we found that activator overexpression can compensate for the loss of SWI/SNF but not for the loss of SAGA.