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The genetics of ageing
- C. Kenyon
- 24 March 2010
The nematode Caenorhabditis elegans ages and dies in a few weeks, but humans can live for 100 years or more, which means that over evolutionary time mutations have increased lifespan more than 2,000-fold.
Genes that act downstream of DAF-16 to influence the lifespan of Caenorhabditis elegans
The findings suggest that the insulin/IGF-I pathway ultimately exerts its effect on lifespan by upregulating a wide variety of genes, including cellular stress-response, antimicrobial and metabolic genes, and by downregulating specific life-shortening genes.
Regulation of Aging and Age-Related Disease by DAF-16 and Heat-Shock Factor
The findings suggest that HSF-1 and DAF-16 together activate expression of specific genes, including genes encoding small heat-shock proteins, which in turn promote longevity, which couple the normal aging process to this type of age-related disease.
A C. elegans mutant that lives twice as long as wild type
Finding that mutations in the gene daf-2 can cause fertile, active, adult Caenorhabditis elegans hermaphrodites to live more than twice as long as wild type raises the possibility that the longevity of the dauer is not simply a consequence of its arrested growth, but instead results from a regulated lifespan extension mechanism that can be uncoupled from other aspects of dauer formation.
daf-16: An HNF-3/forkhead family member that can function to double the life-span of Caenorhabditis elegans.
The wild-type Caenorhabditis elegans nematode ages rapidly, undergoing development, senescence, and death in less than 3 weeks. In contrast, mutants with reduced activity of the gene daf-2, a homolog…
The nematode Caenorhabditis elegans.
- C. Kenyon
- 10 June 1988
In Caenorhabditis elegans patterns of cell division, differentiation, and morphogenesis can be observed with single-cell resolution in intact, living animals. Mechanisms that determine behaviors of…
The Plasticity of Aging: Insights from Long-Lived Mutants
- C. Kenyon
- 25 February 2005
Regulation of the Caenorhabditis elegans longevity protein DAF-16 by insulin/IGF-1 and germline signaling
It is shown that the D AF-2 pathway prevents DAF-16 accumulation in nuclei, and it is found that both sensory neurons and germline activity regulate DAF/IGF-1 signaling, but the nuclear localization patterns are different, which reveal unexpected complexity in the Daf-16-dependent pathways that regulate aging.
Rates of Behavior and Aging Specified by Mitochondrial Function During Development
The developing animal appears to contain a regulatory system that monitors mitochondrial activity early in life and, in response, establishes rates of respiration, behavior, and aging that persist during adulthood.
Lifespan extension by conditions that inhibit translation in Caenorhabditis elegans
- M. Hansen, S. Taubert, D. Crawford, Nataliya Libina, Seung-Jae V. Lee, C. Kenyon
- BiologyAging cell
- 1 February 2007
These findings link TOR, but not sir‐2.1, to the longevity response induced by dietary restriction (DR) in C. elegans, and they suggest that neither TOR inhibition nor DR extends lifespan simply by reducing protein synthesis.