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Molecular and Cellular Biology, April 2008, p. 2509-2516, Vol. 28, No. 8
0270-7306/08/$08.00+0     doi:10.1128/MCB.00658-07
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

Artificial Recruitment of Mediator by the DNA-Binding Domain of Adr1 Overcomes Glucose Repression of ADH2 Expression{triangledown}

Elton T. Young,* Christine Tachibana, Hsin-Wen Ella Chang, Kenneth M. Dombek, Erin M. Arms, and Rhiannon Biddick

Department of Biochemistry, University of Washington, Seattle, Washington 98195-7350

Received 14 April 2007/ Returned for modification 17 October 2007/ Accepted 28 January 2008

The transcription factor Adr1 activates numerous genes in nonfermentable carbon source metabolism. An unknown mechanism prevents Adr1 from stably binding to the promoters of these genes in glucose-grown cells. Glucose depletion leads to Snf1-dependent binding. Chromatin immunoprecipitation showed that the Adr1 DNA-binding domain could not be detected at the ADH2 promoter under conditions in which the binding of the full-length protein occurred. This suggested that an activation domain is required for stable binding, and coactivators may stabilize the interaction with the promoter. Artificial recruitment of Mediator tail subunits by fusion to the Adr1 DNA-binding domain overcame both the inhibition of promoter binding and glucose repression of ADH2 expression. In contrast, an Adr1 DNA-binding domain-Tbp fusion did not overcome glucose repression, although it was an efficient activator of ADH2 expression under derepressing conditions. When Mediator was artificially recruited, ADH2 expression was independent of SNF1, SAGA, and Swi/Snf, whereas ADH2 expression was dependent on these factors with wild-type Adr1. These results suggest that in the presence of glucose, the ADH2 promoter is accessible to Adr1 but that other interactions that occur when glucose is depleted do not take place. Artificial recruitment of Mediator appears to overcome this requirement and to allow stable binding and transcription under normally inhibitory conditions.

* Corresponding author. Mailing address: Department of Biochemistry, Box 357350, University of Washington, Seattle, WA 98195-7350. Phone: (206) 543-6517. Fax: (206) 685-1792. E-mail: ety{at}u.washington.edu

{triangledown} Published ahead of print on 4 February 2008.

Molecular and Cellular Biology, April 2008, p. 2509-2516, Vol. 28, No. 8
0270-7306/08/$08.00+0     doi:10.1128/MCB.00658-07
Copyright © 2008, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Ratnakumar, S., Kacherovsky, N., Arms, E., Young, E. T. (2009). Snf1 Controls the Activity of Adr1 Through Dephosphorylation of Ser230. Genetics 182: 735-745 [Abstract] [Full Text]  
  • Biddick, R. K., Law, G. L., Chin, K. K. B., Young, E. T. (2008). The Transcriptional Coactivators SAGA, SWI/SNF, and Mediator Make Distinct Contributions to Activation of Glucose-repressed Genes. J. Biol. Chem. 283: 33101-33109 [Abstract] [Full Text]  


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