Elevated expression of stress response genes resulting from deletion of the PHO85 gene

Authors

  • Barbara K. Timblin,

    1. Department of Microbiology and Immunology, Allegheny University of the Health Sciences, 2900 Queen Lane, Philadelphia, PA 19129, USA.
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    • Present address: Department of Biochemistry and Molecular Biology, University of Massachusetts, Amherst, MA 01003 4505, USA

  • Lawrence W. Bergman

    1. Department of Microbiology and Immunology, Allegheny University of the Health Sciences, 2900 Queen Lane, Philadelphia, PA 19129, USA.
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Lawrence W. Bergman E-mail bergmanw@auhs.edu; Tel. (215) 991 8376; Fax (215) 848 2271.

Abstract

The cyclin-dependent protein kinase Pho85 is a known negative regulatory factor for two stress response genes, PHO5 and GSY2, which encode the inducible form of acid phosphatase and glycogen synthase, respectively, in the yeast Saccharomyces cerevisiae. Cells carrying a disruption of the PHO85 gene inappropriately express both PHO5 and GSY2, resulting in the increase in phosphate scavenging and hyperaccumulation of glycogen in nutrient-rich conditions. Constitutive activation of PKA in a pho85 mutant suppresses the hyperaccumulation of glycogen. This work presents data to show that, at least in part, the suppression of glycogen biosynthesis upon activation of PKA in a pho85 mutant results from the suppression of GSY2 expression. In addition to GSY2, disruption of the PHO85 gene inappropriately triggers the derepression of two other stress response genes, HSP12 and UBI4. At least in the case of GSY2, regulation of transcription by Pho85 is not through the stress-responsive cis-promoter elements (STRE). Furthermore, Pho85 may associate with the known cyclin Pho80 in the transcriptional regulation of these genes.

Footnotes

  1. Present address: Department of Biochemistry and Molecular Biology, University of Massachusetts, Amherst, MA 01003 4505, USA

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