The yeast mic2 mutant is defective in the formation of mannosyl‐diinositolphosphorylceramide

FEBS Letters

Fischer, Petra¹  Schneiter, Roger¹  Daum, Günther¹  Leber, Andrea¹  Kohlwein, Sepp D.¹ 

[1] Institut für Biochemie und Lebensmittelchemie, Technische Universität Graz, A-8010 Graz, Austria

关键词: Saccharomyces cerevisiae;    Yeast;    Sphingolipid;    Plasma membrane;    Nystatin;    Inositol;    IPC;    inositolphosphorylceramide;    MIPC;    mannosyl-inositolphosphorylceramide;    M(IP)2C;    mannosyl-diinositolphosphorylceramide;    PI;    phosphatidylinositol;    TMA-DPH;    trimethylamino-diphenyl-1;    3;    5-hexatriene;   

DOI  :  10.1016/S0014-5793(97)00692-3

学科分类：生物化学/生物物理

来源: John Wiley & Sons Ltd.

【 摘 要 】

The mic2 mutation dominantly blocks formation of mannosyl-diinositolphosphorylceramide, the most abundant sphingolipid of the yeast, Saccharomyces cerevisiae. Interestingly, lack of mannosyl-diinositolphosphorylceramide is not lethal but is compensated for by increased amounts of inositolphosphorylceramide and mannosyl-inositolphosphorylceramide in the plasma membrane and Golgi of the mutant. The level of negatively charged phospholipids in the plasma membrane of the mic2 strain is markedly reduced; the sterol composition is not altered. In spite of dramatic changes of its lipid composition the mutant grows like wild type on complex and minimal media, under osmotic stress conditions, at low pH, and in the presence of high ionic strength. While sensitivity to several drugs is not altered, the mic2 mutant strain becomes resistant to the polyene antibiotic nystatin.

【 授权许可】

Unknown