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Genetics. 2016 Nov;204(3):905-920. doi: 10.1534/genetics.116.192369. Epub 2016 Sep 16.

Different Mechanisms of Longevity in Long-Lived Mouse and Caenorhabditis elegans Mutants Revealed by Statistical Analysis of Mortality Rates.

Author information

1
Department of Biology, McGill University, Montreal, Quebec H3A 1B1, Canada.
2
Department of Biology, McGill University, Montreal, Quebec H3A 1B1, Canada siegfried.hekimi@mcgill.ca.

Abstract

Mouse and Caenorhabditis elegans mutants with altered life spans are being used to investigate the aging process and how genes determine life span. The survival of a population can be modeled by the Gompertz function, which comprises two parameters. One of these parameters ("G") describes the rate at which mortality accelerates with age and is often described as the "rate of aging." The other parameter ("A") may correspond to the organism's baseline vulnerability to deleterious effects of disease and the environment. We show that, in mice, life-span-extending mutations systematically fail to affect the age-dependent acceleration of mortality (G), but instead affect only baseline vulnerability (A). This remains true even when comparing strains maintained under identical environmental conditions. In contrast, life-span-extending mutations in C. elegans were associated with decreases in G These observations on mortality rate kinetics suggest that the mechanisms of aging in mammals might fundamentally differ from those in nematodes.

KEYWORDS:

Caenorhabditis elegans; Gompertz; aging; longevity; mice

PMID:
27638422
PMCID:
PMC5105868
DOI:
10.1534/genetics.116.192369
[Indexed for MEDLINE]
Free PMC Article

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