Mammalian Bax triggers apoptotic changes in yeast

FEBS Letters

Fröhlich, Eleonore³  Madeo, Frank¹  Hilt, Wolfgang²  Fröhlich, Kai-Uwe¹  Wolf, Dieter H²  Ligr, Martin² 

[1] Physiologisch-Chemisches Institut, Universität Tübingen, Hoppe-Seyler-Straße 4, 72076 Tübingen, Germany;Institut für Biochemie, Universität Stuttgart, Pfaffenwaldring 55, 70569 Stuttgart, Germany;Anatomisches Institut, Universität Tübingen, Österbergstraße 3, 72074 Tübingen, Germany

关键词: Apoptosis;    Bax;    Yeast Saccharomyces cerevisiae;    DAPI;    diaminophenylindole;    PI;    propidium iodide;    PS;    phosphatidylserine;    SC;    synthetic complete growth medium;    TUNEL;    terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling;   

DOI  :  10.1016/S0014-5793(98)01227-7

学科分类：生物化学/生物物理

来源: John Wiley & Sons Ltd.

【 摘 要 】

Apoptosis is co-regulated by the conserved family of Bcl-2-related proteins, which includes both its agonists (Bax) and antagonists (Bcl-X_L). A mutant strain of the yeast Saccharomyces cerevisiae has been shown to express all morphological signs of apoptosis. Overexpression of Bax is lethal in S. cerevisiae, whereas simultaneous overexpression of Bcl-X_L rescues the cells. We report that overexpression of mammalian Bax in a S. cerevisiae wild type strain triggers morphological changes similar to those of apoptotic metazoan cells: the loss of asymmetric distribution of plasma membrane phosphatidylserine, plasma membrane blebbing, chromatin condensation and margination, and DNA fragmentation. Simultaneous overexpression of Bcl-X_L prevents these changes. We demonstrate that Bax triggers phenotypic alterations in yeast strongly resembling those it causes in metazoan apoptotic cells.

【 授权许可】

Unknown