Ageing of biological systems is accompanied by alterations in mitochondrial morphology, including a transformation from networks and filaments to punctuate units¹. The significance of these alterations with regard to ageing is not known. Here, we demonstrate that the dynamin-related protein 1 (Dnm1p), a mitochondrial fission protein conserved from yeast to humans², affects ageing in the two model systems we studied, Podospora anserina and Saccharomyces cerevisiae. Deletion of the Dnm1 gene delays the transformation of filamentous to punctuate mitochondria and retards ageing without impairing fitness and fertility typically observed in long-lived mutants. Our data further suggest that reduced mitochondrial fission extends life span by increasing cellular resistance to the induction of apoptosis and links mitochondrial dynamics, apoptosis and life-span control.

1. Johann Wolfgang Goethe University, Institute of Molecular Biosciences, Max-von-Laue-Str. 9, 60438 Frankfurt, Germany.
2. Göteborg University, Department of Cell and Molecular Biology, Medicinaregatan 9C, 413 90 Göteborg, Sweden

Correspondence to: H.D. Osiewacz¹ e-mail: osiewacz@bio.uni-frankfurt.de

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