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Snf1-independent, glucose-resistant transcription of Adr1-dependent genes in a mediator mutant of Saccharomyces cerevisiae.

Glucose represses transcription of a network of co-regulated genes in Saccharomyces cerevisiae, ensuring that it is utilized before poorer carbon sources are metabolized. Adr1 is a glucose-regulated transcription factor whose promoter binding and activity require Snf1, the yeast homologue of the AMP-activated protein kinase in higher eukaryotes. In this study we found that a temperature-sensitive allele of MED14, a Mediator middle subunit that tethers the tail to the body, allowed a low level of Adr1-independent ADH2 expression that can be enhanced by Adr1 in a dose-dependent manner. A low level of TATA-independent ADH2 expression was observed in the med14-truncated strain and transcription of ADH2 and other Adr1-dependent genes occurred in the absence of Snf1 and chromatin remodeling coactivators. Loss of ADH2 promoter nucleosomes had occurred in the med14 strain in repressing conditions and did not require ADR1. A global analysis of transcription revealed that loss of Med14 function was associated with both up- and down- regulation of several groups of co-regulated genes, with ADR1-dependent genes being the most highly represented in the upregulated class. Expression of most genes was not significantly affected by the loss of Med14 function.

Pubmed ID: 19732343


  • Young ET
  • Yen K
  • Dombek KM
  • Law GL
  • Chang E
  • Arms E


Molecular microbiology

Publication Data

October 21, 2009

Associated Grants

  • Agency: NIGMS NIH HHS, Id: GM26079
  • Agency: NIGMS NIH HHS, Id: R01 GM026079

Mesh Terms

  • Alcohol Dehydrogenase
  • DNA, Fungal
  • DNA-Binding Proteins
  • Gene Expression Profiling
  • Gene Expression Regulation, Fungal
  • Glucose
  • Mediator Complex
  • Nucleosomes
  • Oligonucleotide Array Sequence Analysis
  • Promoter Regions, Genetic
  • Protein-Serine-Threonine Kinases
  • Saccharomyces cerevisiae
  • Saccharomyces cerevisiae Proteins
  • Transcription Factors
  • Transcription, Genetic