DELETION OF THE GENE ENCODING THE CYCLIN-DEPENDENT PROTEIN-KINASE PHO85 ALTERS GLYCOGEN-METABOLISM IN SACCHAROMYCES-CEREVISIAE

Pho85, a protein kinase with significant homology to the cyclin-depend ent kinase, Cdc28, has been shown to function in repression of transcr iption 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 de scribe several unique phenotypes associated with the deletion of the P HO85 gene including growth defects on a variety of carbon sources and hyperaccumulation of glycogen in rich medium high in Pi. Hyperaccumula tion of glycogen in the pho85 strains is independent of other APase re gulatory molecules and is not signaled through Snfl kinase. However, c onstitutive activation of cAPK suppresses the hyperaccumulation of gly cogen in a pho85 mutant. Mutation of the type-1 protein phosphatase en coded 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 evide nce that Pho85 has functions in addition to transcriptional regulation of APase and cell-cycle progression including the regulation of glyco gen levels in the cell and may provide a link between the nutritional state of the cell and these growth related responses.