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  On the relevance of mitochondrial fusions for the accumulation of mitochondrial deletion mutants: A modelling study

Kowald, A., Jendrach, M., Pohl, S., Bereiter-Hahn, J., & Hammerstein, P. (2005). On the relevance of mitochondrial fusions for the accumulation of mitochondrial deletion mutants: A modelling study. Aging Cell, 4(5), 273-283. doi:10.1111/j.1474-9726.2005.00169.x.

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Kowald et al. - Aging Cell.pdf (Any fulltext), 252KB
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Kowald, Axel1, Author              
Jendrach, Marina, Author
Pohl, Sandra, Author
Bereiter-Hahn, Jürgen, Author
Hammerstein, Peter, Author
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1Independent Junior Research Groups (OWL), Max Planck Institute for Molecular Genetics, Max Planck Society, ou_1433554              

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 Abstract: The molecular mechanisms underlying the aging process are still unclear, but the clonal accumulation of mitochondrial deletion mutants is one of the prime candidates. An important question for the mitochondrial theory of aging is to discover how defective organelles might be selected at the expense of wild-type mitochondria. We propose that mitochondrial fission and fusion events are of critical importance for resolving this apparent contradiction. We show that the occurrence of fusions removes the problems associated with the idea that smaller DNA molecules accumulate because they replicate in a shorter time – the survival of the tiny (SOT) hypothesis. Furthermore, stochastic simulations of mitochondrial replication, mutation and degradation show that two important experimental findings, namely the overall low mosaic pattern of oxidative phosphorylation (OXPHOS) impaired cells in old organisms and the distribution of deletion sizes, can be reproduced and explained by this hypothesis. Finally, we make predictions that can be tested experimentally to further verify our explanation for the age-related accumulation of mitochondrial deletion mutants.

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Language(s): eng - English
 Dates: 2005-10
 Publication Status: Published in print
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 Identifiers: eDoc: 271997
DOI: 10.1111/j.1474-9726.2005.00169.x
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Title: Aging Cell
Source Genre: Journal
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Pages: - Volume / Issue: 4 (5) Sequence Number: - Start / End Page: 273 - 283 Identifier: ISSN: 1474-9718