Fitness cost of extended lifespan in Caenorhabditis elegans.
An insulin/IGF-I-like signalling pathway determines the rate of aging of the adult nematode, Caenorhabditis elegans. Mutations in genes encoding this pathway can result in a doubling of lifespan. While such mutations may appear to have little effect on development or fertility, evolutionary theory predicts that large increases in lifespan will not be optimal for fitness. We demonstrate by laboratory natural selection that partial loss of function of the insulin receptor-like protein DAF-2 results in dramatically reduced fitness even under laboratory conditions. Despite long-lived mutants appearing healthy, they exhibit a heavy fitness cost consistent with an evolutionary theory of aging.
Jenkins
Nicole L
NL
Buck Institute for Age Research, 8001 Redwood Boulevard, Novato, CA 94945, USA. njenkins@buckinstitute.org
McColl
Gawain
G
Lithgow
Gordon J
GJ
D000375:Aging / Q000235:genetics*; D000818:Animals; D017173:Caenorhabditis elegans / Q000235:genetics* / Q000502:physiology; D029742:Caenorhabditis elegans Proteins; D005508:Food Deprivation / Q000502:physiology; D005787:Gene Frequency; D008136:Longevity / Q000235:genetics* / Q000502:physiology; D008957:Models, Genetic; D009154:Mutation / Q000235:genetics; D011972:Receptor, Insulin / Q000235:genetics*; D012098:Reproduction / Q000235:genetics; D012641:Selection, Genetic; D015398:Signal Transduction / Q000235:genetics*
D029742:Caenorhabditis elegans Proteins; C107483:DAF-2 protein, C elegans; D011972:Receptor, Insulin