Alterations in mitochondrial morphology of Schizosaccharomyces pombe induced by cell-death promoting agents
Jazyk angličtina Země Spojené státy americké Médium print
Typ dokumentu časopisecké články, práce podpořená grantem
PubMed
18062187
DOI
10.1007/bf02932093
Knihovny.cz E-zdroje
- MeSH
- buněčná smrt účinky léků fyziologie MeSH
- DNA fungální genetika MeSH
- fluorescenční mikroskopie MeSH
- karbocyaniny chemie MeSH
- kyselina octová farmakologie MeSH
- mitochondriální DNA genetika MeSH
- mitochondrie účinky léků fyziologie ultrastruktura MeSH
- plazmidy genetika MeSH
- protein X asociovaný s bcl-2 biosyntéza genetika fyziologie MeSH
- Schizosaccharomyces účinky léků genetika fyziologie MeSH
- Southernův blotting MeSH
- transformace genetická MeSH
- zelené fluorescenční proteiny biosyntéza genetika MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- Názvy látek
- 3,3'-dihexyl-2,2'-oxacarbocyanine MeSH Prohlížeč
- DNA fungální MeSH
- karbocyaniny MeSH
- kyselina octová MeSH
- mitochondriální DNA MeSH
- protein X asociovaný s bcl-2 MeSH
- zelené fluorescenční proteiny 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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