Yeast Genetics and Molecular Biology 2000
University of Washington
Seattle, Washington USA
July 2000


Name: Kuchin, Sergei
Mailing Address: Inst. of Cancer Research, Columbia University, 701 West 168th St., New York, NY 10032, USA
Email Address: svk4@columbia.edu
Phone & FAX numbers: (212)305-3851 & (212)305-1741

#043

A regulatory shortcut between the Snf1 protein kinase and RNA polymerase II holoenzyme.
Sergei Kuchin (1), Isabelle Treich (2), Marian Carlson (1)
(1) Inst. of Cancer Research, Columbia University, 701 West 168th St., New York, NY 10032, USA; (2) Present address: ValiGene, Tour Neptune, 92086, Paris la Defense, France

RNA polymerase II holoenzymes respond to transcriptional activators and repressors that are regulated by signaling pathways. We present evidence for a 'shortcut' mechanism in which the Snf1 protein kinase of the glucose signaling pathway directly regulates transcription by the yeast holoenzyme. First, in response to glucose limitation, the Snf1 kinase stimulates transcription by holoenzyme that has been artificially recruited to a reporter by a LexA fusion to a holoenzyme component. Second, Snf1 interacts physically with Srb/mediator proteins of the holoenzyme in both two-hybrid and coimmunoprecipitation assays. Third, a catalytically hyperactive Snf1, when bound to a promoter as a LexA fusion protein, activates transcription in a glucose-regulated manner; moreover, this activation is dependent on the integrity of the Srb/mediator complex. These results suggest that direct regulatory interactions between signal transduction pathways and RNA polymerase II holoenzyme provide a mechanism for transcriptional control in response to important signals.


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