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

FEBS Letters

Roach, Peter.J¹  Wilson, Wayne A¹  Wang, Zhong¹ 

[1] Department of Biochemistry and Molecular Biology and Center for Diabetes Research, Indiana University School of Medicine, 635 Barnhill Drive, Indianapolis, IN 46202-5122, USA

关键词: Glycogen;    Cyclin-dependent protein kinase;    PHO85;    COQ3;    Respiratory mutant;   

DOI  :  10.1016/S0014-5793(02)02448-1

学科分类：生物化学/生物物理

来源: John Wiley & Sons Ltd.

【 摘 要 】

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.

【 授权许可】

Unknown