Animals vary dramatically in lifespan, but why is not clear. Here Johan Auwerx and colleagues report how natural variation in mitochondrial ribosome protein expression translates to lifespan extension in mice and worms, and suggest a unified mechanism behind the effects of metabolic perturbations on longevity. They looked for genetic variation linked to longevity in the BXD genetic reference population of inbred mouse strains. Longevity mapped to mitochondrial ribosomal proteins. Using mouse population genetics and RNA interference experiments in Caenorhabditis elegans, mitochondrial ribosomal protein S5 (Mrps5) and other mitochondrial ribosomal proteins were identified as metabolic and longevity regulators.
- Beneficial miscommunication (News & Views p442, doi: 10.1038/497442a)
- Mitonuclear protein imbalance as a conserved longevity mechanism (Article p451, doi: 10.1038/nature12188)
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