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Mitochondria, maternal inheritance, and asymmetric fitness: Why males die younger

Authors

  • Jonci N. Wolff,

    1. School of Biotechnology and Biomolecular Sciences, University of New South Wales, Sydney, NSW, Australia
    2. Evolution and Ecology Research Centre, University of New South Wales, Sydney, NSW, Australia
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  • Neil J. Gemmell

    Corresponding author
    1. Department of Anatomy, Centre for Reproduction and Genomics, University of Otago, Dunedin, New Zealand
    2. Allan Wilson Centre for Molecular Ecology and Evolution, University of Otago, Dunedin, New Zealand
    • Department of Anatomy, Centre for Reproduction and Genomics, University of Otago, Dunedin, New Zealand.
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Abstract

Mitochondrial function is achieved through the cooperative interaction of two genomes: one nuclear (nuDNA) and the other mitochondrial (mtDNA). The unusual transmission of mtDNA, predominantly maternal without recombination is predicted to affect the fitness of male offspring. Recent research suggests the strong sexual dimorphism in aging is one such fitness consequence. The uniparental inheritance of mtDNA results in a selection asymmetry; mutations that affect only males will not respond to natural selection, imposing a male-specific mitochondrial mutation load. Prior work has implicated this male-specific mutation load in disease and infertility, but new data from fruit flies suggests a prominent role for mtDNA in aging; across many taxa males almost invariably live shorter lives than females. Here we discuss this new work and identify some areas of future research that might now be encouraged to explore what may be the underpinning cause of the strong sexual dimorphism in aging.

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