Lookup NU author(s): Dr Axel Kowald,
Emeritus Professor Thomas Kirkwood
This work is licensed under a Creative Commons Attribution 4.0 International License (CC BY 4.0).
© 2018 by the authors. Licensee MDPI, Basel, Switzerland. Mitochondria are cell organelles that are special since they contain their own genetic material in the form of mitochondrial DNA (mtDNA). Damage and mutations of mtDNA are not only involved in several inherited human diseases but are also widely thought to play an important role during aging. In both cases, point mutations or large deletions accumulate inside cells, leading to functional impairment once a certain threshold has been surpassed. In most cases, it is a single type of mutant that clonally expands and out-competes the wild type mtDNA, with different mutant molecules being amplified in different cells. The challenge is to explain where the selection advantage for the accumulation comes from, why such a large range of different deletions seem to possess this advantage, and how this process can scale to species with different lifespans such as those of rats and man. From this perspective, we provide an overview of current ideas, present an update of our own proposal, and discuss the wider relevance of the phenomenon for aging.
Author(s): Kowald A, Kirkwood TBL
Publication type: Article
Publication status: Published
Online publication date: 27/02/2018
Acceptance date: 16/02/2018
Date deposited: 19/03/2018
ISSN (print): 2073-4425
ISSN (electronic): 2073-4425
Publisher: MDPI AG
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