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Deletion of the Gene Encoding the Cyclin-Dependent Protein Kinase Pho85 Alters Glycogen Metabolism in Saccharomyces cerevisiae
Journal article   Open access   Peer reviewed

Deletion of the Gene Encoding the Cyclin-Dependent Protein Kinase Pho85 Alters Glycogen Metabolism in Saccharomyces cerevisiae

Barbara K Timblin, Kelly Tatchell and Lawrence W Bergman
Genetics (Austin), v 143(1)
01 May 1996
PMID: 8722762
url
https://doi.org/10.1093/genetics/143.1.57View
Published, Version of Record (VoR) Open

Abstract

Abstract Pho85, a protein kinase with significant homology to the cyclin-dependent kinase, Cdc28, has been shown to function in repression of transcription of acid phosphatase (APase, encoded by PHO5) in high phosphate (Pi) medium, as well as in regulation of the cell cycle at G1/S. We describe several unique phenotypes associated with the deletion of the PHO85 gene including growth defects on a variety of carbon sources and hyperaccumulation of glycogen in rich medium high in Pi. Hyperaccumulation of glycogen in the pho85 strains is independent of other APase regulatory molecules and is not signaled through Snf1 kinase. However, constitutive activation of cAPK suppresses the hyperaccumulation of glycogen in a pho85 mutant. Mutation of the type-1 protein phosphatase encoded by GLC7 only partially suppresses the glycogen phenotype of the pho85 mutant. Additionally, strains containing a deletion of the PHO85 gene show an increase in expression of GSY2. This work provides evidence that Pho85 has functions in addition to transcriptional regulation of APase and cell-cycle progression including the regulation of glycogen levels in the cell and may provide a link between the nutritional state of the cell and these growth related responses.

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Collaboration types
Domestic collaboration
Web of Science research areas
Genetics & Heredity
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