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Genome Biology volume 2, Article number: spotlight-20010410-01 (2001)
Mutations that increase the life span of Caenorhabditis elegans encode components of the insulin/IGF signalling pathway. In the April 6 Science, two papers describe mutations that link insulin signaling with longevity in Drosophila melanogaster. Clancy et al. report that homozygous null mutations in chico, encoding an insulin receptor substrate protein, increased the female fly life span by up to 48% (Science 2001, 292:104-106). They were able to demonstrate that the effects of chico on longevity could be separated from effects on fertility, stress resistance or body size. Tatar et al. show that the Drosophila InR (insulin-like receptor), which is a homolog of the C. elegans daf-2 gene, also regulates adult longevity (Science 2001, 292:107-110). Female flies with heteroallelic combinations of hypomorphic InR alleles lived up to 85% longer than controls. Tatar et al. provide evidence that the effects of InR are mediated by regulation of neuroendocrine function and juvenile hormone production. The conservation of insulin signalling pathways suggests that similar genes may affect longevity and aging in mammals.
Genetic pathways that regulate ageing in model organisms.
Autonomous control of cell and organ size by CHICO, a Drosophila homolog of vertebrate IRS1-4.
A heady message for lifespan regulation.
Pleiotropic effects of growth hormone and insulin-like growth factor (IGF)-1 on biological aging: inferences from moderate caloric-restricted animals.
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Weitzman, J.B. Long-lived flies. Genome Biol 2, spotlight-20010410-01 (2001) doi:10.1186/gb-spotlight-20010410-01
- Life Span
- Insulin Receptor
- Insulin Signaling
- Caenorhabditis Elegans
- Null Mutation