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Cell Cycle. 2015;14(11):1698-703. doi: 10.1080/15384101.2015.1029685.

Inhibition of peroxisome fission, but not mitochondrial fission, increases yeast chronological lifespan.

Author information

1
a Molecular Cell Biology, Systems Biology Center for Energy Metabolism and Aging; Groningen Biomolecular Sciences and Biotechnology Institute; University of Groningen ; Groningen , The Netherlands.

Abstract

Mitochondria are key players in aging and cell death. It has been suggested that mitochondrial fragmentation, mediated by the Dnm1/Fis1 organelle fission machinery, stimulates aging and cell death. This was based on the observation that Saccharomyces cerevisiae Δdnm1 and Δfis1 mutants show an enhanced lifespan and increased resistance to cell death inducers. However, the Dnm1/Fis1 fission machinery is also required for peroxisome division. Here we analyzed the significance of peroxisome fission in yeast chronological lifespan, using yeast strains in which fission of mitochondria was selectively blocked. Our data indicate that the lifespan extension caused by deletion of FIS1 is mainly due to a defect in peroxisome fission and not caused by a block in mitochondrial fragmentation. These observations are underlined by our observation that deletion of FIS1 does not lead to lifespan extension in yeast peroxisome deficient mutant cells.

KEYWORDS:

Fis1; chronological aging; fission; mitochondria; peroxisome; yeast

PMID:
25840089
PMCID:
PMC4614869
DOI:
10.1080/15384101.2015.1029685
[Indexed for MEDLINE]
Free PMC Article

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