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Mammalian Bax triggers apoptotic changes in yeast
1Institut für Biochemie, Universität Stuttgart, Germany.
FEBS Letters
|November 20, 1998
Summary
Overexpressing mammalian Bax in yeast triggers apoptosis-like changes. Co-expressing Bcl-X(L) prevents these effects, demonstrating Bax
Area of Science:
- Cell Biology
- Molecular Biology
- Yeast Genetics
Background:
- Apoptosis (programmed cell death) is regulated by Bcl-2 family proteins.
- Bcl-2 proteins include agonists like Bax and antagonists like Bcl-X(L).
- Previous studies showed a mutant yeast strain exhibits apoptosis-like features.
Purpose of the Study:
- To investigate the effects of mammalian Bax overexpression in wild-type yeast.
- To determine if Bcl-X(L) can counteract Bax-induced apoptosis-like phenotypes in yeast.
- To establish yeast as a model for studying metazoan apoptosis regulation.
Main Methods:
- Overexpression of mammalian Bax and Bcl-X(L) in Saccharomyces cerevisiae.
- Microscopic analysis of cellular morphology.
- Assessment of plasma membrane phosphatidylserine distribution.
- Analysis of chromatin condensation and DNA fragmentation.
Main Results:
- Overexpression of Bax induced apoptosis-like morphological changes in yeast.
- Observed changes included loss of plasma membrane asymmetry, blebbing, and DNA fragmentation.
- Simultaneous overexpression of Bcl-X(L) completely prevented these Bax-induced alterations.
Conclusions:
- Mammalian Bax can induce apoptosis-like phenotypes in wild-type yeast.
- Bcl-X(L) acts as an antagonist, suppressing Bax-mediated cell death in yeast.
- Yeast serves as a valuable model for studying conserved mechanisms of apoptosis.