Natural selection: Evolution of lifespan in C. elegans

@article{Walker2000NaturalSE,
  title={Natural selection: Evolution of lifespan in C. elegans},
  author={David W. Walker and Gawain McColl and Nicole L. Jenkins and Jennifer M. Harris and Gordon J. Lithgow},
  journal={Nature},
  year={2000},
  volume={405},
  pages={296-297}
}
It was proposed almost 50 years ago that ageing is non-adaptive and is the consequence of a decline in the force of natural selection with age. This led to the theory that ageing results from detrimental effects late in life of genes that act beneficially in early life, so any genetic alteration that increases lifespan might be expected to reduce fitness, for example. We show here that a mutation that greatly increases the lifespan of the nematode Caenorhabditis elegans does indeed exhibit a… Expand

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References

SHOWING 1-10 OF 10 REFERENCES
A C. elegans mutant that lives twice as long as wild type
TLDR
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. Expand
Thermotolerance and extended life-span conferred by single-gene mutations and induced by thermal stress.
TLDR
The results suggest that ability to respond to stress limits the life expectancy of C. elegans and might do so in other metazoa as well, and the relationship between increased thermotolerance and increased life-span is investigated. Expand
Movement as an index of vitality: comparing wild type and the age-1 mutant of Caenorhabditis elegans.
  • S. A. Duhon, T. Johnson
  • Biology, Medicine
  • The journals of gerontology. Series A, Biological sciences and medical sciences
  • 1995
TLDR
Cumulative lifetime movements of individuals were highly correlated with, and thus a good predictor of, individual life span, and imply that the physiological process altered by the age-1 mutation results in increased health during later life as monitored by increased ability to move. Expand
Genetic analysis of the roles of daf-28 and age-1 in regulating Caenorhabditis elegans dauer formation.
TLDR
Daf-28(sa191) acts at a novel point downstream in the genetic pathway for dauer formation and causes a modest increase in life span, which is most similar to those of daf-2 and Daf-23 mutations, which also cause a dramatic increase inLife span. Expand
An insulin-like signaling pathway affects both longevity and reproduction in Caenorhabditis elegans.
TLDR
Insulin signaling, mediated by DAF-2 through the AGE-1 phosphatidylinositol-3-OH kinase, regulates reproduction and embryonic development, as well as dauer diapause and life span, and that Daf-16 transduces these signals. Expand
Thermotolerance of a long-lived mutant of Caenorhabditis elegans.
TLDR
It is proposed that the enhanced ability of Age strains to cope with environmental stress may be mechanistically related to their lower age-specific mortality rates. Expand
PLEIOTROPY, NATURAL SELECTION, AND THE EVOLUTION OF SENESCENCE
  • George C. Williams
  • Biology
  • 1957
form the much simpler task of merely maintaining what is already formed. It is true, of course, that some parts of organisms do literally wear out. Human teeth, for instance, show wear similar toExpand
A phosphatidylinositol-3-OH kinase family member regulating longevity and diapause in Caenorhabditis elegans
TLDR
It is suggested that phosphatidylinositol signalling mediated by AGE-1 protein controls lifespan and the dauer diapause decision. Expand
Three mutants that extend both mean and maximum life span of the nematode, Caenorhabditis elegans, define the age-1 gene.
TLDR
Three of four mutant strains studied in the nematode Caenorhabditis elegans contain recessive mutations that significantly lengthen life; MK542 and MK546 consistently fail to complement the long life phenotype of age-1 and are therefore allelic. Expand
UNSOLVED problem of biology.
  • P. Medawar
  • Medicine, Biology
  • The Medical journal of Australia
  • 1953