Prospects & Overviews
Mitochondria, maternal inheritance, and asymmetric fitness: Why males die younger
Article first published online: 27 DEC 2012
Copyright © 2013 WILEY Periodicals, Inc.
Volume 35, Issue 2, pages 93–99, February 2013
How to Cite
Wolff, J. N. and Gemmell, N. J. (2013), Mitochondria, maternal inheritance, and asymmetric fitness: Why males die younger. Bioessays, 35: 93–99. doi: 10.1002/bies.201200141
- Issue published online: 15 JAN 2013
- Article first published online: 27 DEC 2012
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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