HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

J. Biol. Chem., Vol. 282, Issue 52, 37308-37315, December 28, 2007

This Article Full Text Full Text (PDF) Supplemental Data All Versions of this Article: 282/52/37308    most recent M707363200v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Tachibana, C. Articles by Young, E. T. Search for Related Content PubMed PubMed Citation Articles by Tachibana, C. Articles by Young, E. T. Related Collections Papers Of The Week Social Bookmarking                      What's this?

A Poised Initiation Complex Is Activated by SNF1^*

From the Department of Biochemistry, University of Washington, Seattle, Washington 98195

Snf1, the yeast AMP kinase homolog, is essential for derepression of glucose-repressed genes that are activated by Adr1. Although required for Adr1 DNA binding, the precise role of Snf1 is unknown. Deletion of histone deacetylase genes allowed constitutive promoter binding of Adr1 and Cat8, another activator of glucose-repressed genes. In repressed conditions, at the Adr1-and Cat8-dependent ADH2 promoter, partial chromatin remodeling had occurred, and the activators recruited a partial preinitiation complex that included RNA polymerase II. Transcription did not occur, however, unless Snf1 was activated, suggesting a Snf1-dependent event that occurs after RNA polymerase II recruitment. Glucose regulation persisted because shifting to low glucose increased expression. Glucose repression could be completely relieved by combining the three elements of 1) chromatin perturbation by mutation of histone deacetylases, 2) activation of Snf1, and 3) the addition of an Adr1 mutant that by itself confers only weak constitutive activity.

Received for publication, September 4, 2007 , and in revised form, October 4, 2007.

^* This work was supported by NIGMS Grants 26079 and NIDDK67276 (to E. T. Y.) and by NIGMS Grant PHS NRSA T32 GM07270 (to R. K. B.). The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement"in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

The on-line version of this article (available at http://www.jbc.org) contains two supplemental figures and two tables.

This article was selected as a Paper of the Week.

¹ To whom correspondence should be addressed: Dept of Biochemistry, Box 357350, University of Washington, Seattle, WA 98195-7350; Fax: 206-685-1792; E-mail: ety{at}u.washington.edu.

CiteULike    Complore    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this?

This article has been cited by other articles:

				E. T. Young, C. Tachibana, H.-W. E. Chang, K. M. Dombek, E. M. Arms, and R. Biddick Artificial Recruitment of Mediator by the DNA-Binding Domain of Adr1 Overcomes Glucose Repression of ADH2 Expression Mol. Cell. Biol., April 15, 2008; 28(8): 2509 - 2516. [Abstract] [Full Text] [PDF]