Analysis of respiratory mutants reveals new aspects of the control of glycogen accumulation by the cyclin-dependent protein kinase Pho85p

Wayne A. Wilson, Zhong Wang, P. J. Roach

Research output: Contribution to journalArticle

4 Scopus citations

Abstract

The PHO85 gene of Saccharomyces cerevisiae encodes a cyclin-dependent protein kinase that can interact with 10 different cyclins (Pcls). In conjunction with Pcl8p and Pcl10p, Pho85p phosphorylates and regulates glycogen synthase. Respiratory-deficient strains, such as coq3 mutants, have reduced glycogen stores and contain hyperphosphorylated and inactive glycogen synthase. We show here that pho85 coq3 mutants have dephosphorylated and active glycogen synthase yet do not maintain glycogen reserves. In contrast, deletion of PCL8 and PCL10 in the coq3 mutant background partially restores glycogen accumulation. This suggested the existence of inputs from Pho85p into glycogen storage, independent of Pcl8p and Pcl10p, and acting antagonistically.

Original languageEnglish (US)
Pages (from-to)104-108
Number of pages5
JournalFEBS Letters
Volume515
Issue number1-3
DOIs
StatePublished - Mar 27 2002

Keywords

  • COQ3
  • Cyclin-dependent protein kinase
  • Glycogen
  • PHO85
  • Respiratory mutant

ASJC Scopus subject areas

  • Biochemistry
  • Biophysics
  • Molecular Biology

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