Alterations in mitochondrial morphology of Schizosaccharomyces pombe induced by cell-death promoting agents
Language English Country United States Media print
Document type Journal Article, Research Support, Non-U.S. Gov't
PubMed
18062187
DOI
10.1007/bf02932093
Knihovny.cz E-resources
- MeSH
- Cell Death drug effects physiology MeSH
- DNA, Fungal genetics MeSH
- Microscopy, Fluorescence MeSH
- Carbocyanines chemistry MeSH
- Acetic Acid pharmacology MeSH
- DNA, Mitochondrial genetics MeSH
- Mitochondria drug effects physiology ultrastructure MeSH
- Plasmids genetics MeSH
- bcl-2-Associated X Protein biosynthesis genetics physiology MeSH
- Schizosaccharomyces drug effects genetics physiology MeSH
- Blotting, Southern MeSH
- Transformation, Genetic MeSH
- Green Fluorescent Proteins biosynthesis genetics MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Names of Substances
- 3,3'-dihexyl-2,2'-oxacarbocyanine MeSH Browser
- DNA, Fungal MeSH
- Carbocyanines MeSH
- Acetic Acid MeSH
- DNA, Mitochondrial MeSH
- bcl-2-Associated X Protein MeSH
- Green Fluorescent Proteins MeSH
The effect of the yeast cell-death inducing agents, Bax and acetic acid, on mitochondrial structure of Schizosaccharomyces pombe was studied. Comparison of mitochondrial structures in cells grown on different substrates and visualized with different probes revealed variations in their morphology. Cells grown on respiratory C sources as well as in the presence of antimycin A exhibited punctuated mitochondria when visualized with mitochondrially targeted green fluorescent protein, while they still appeared as tubular structures when stained with DiOC6(3). Both expression of Bax and acetic acid treatment induced fragmentation and aggregation of mitochondrial network, which could be prevented by coexpression of Bcl-XL. Aberrant mitochondrial morphology generated by either Bax or acetic acid was not accompanied with the loss of mitochondrial genome (mtDNA), indicating that alterations of mitochondrial morphology following death stimuli follow different mechanisms than those involved in mitochondrial inheritance mutants.
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