A heady message for lifespan regulation.
Mutant Caenorhabditis elegans in which the age-1 and daf-2 genes (involved in insulin-receptor-like signalling) are expressed at low levels exhibit extended lifespan. Wolkow and colleagues recently showed that restricted re-expression of age-1 and daf-2 genes in neurons of these mutants rescues wild-type lifespan as effectively as ubiquitous re-expression. Low levels of insulin-like signalling in neurons might control longevity by enhancing protection against free radical damage. However, in mammalian cells (including neurons) reduced insulin-like signalling is generally thought to be deleterious to antioxidant defence and to neuron survival. Here we discuss the new work and several hypotheses to explain this apparent contradiction.
Dept of Anatomy and Developmental Biology, Royal Free and University College Medical School, Royal Free Campus, Rowland Hill St, London, UK NW3 2PF. tcowen@rfc.ucl.ac.uk
T
T
Cowen
D000818:Animals; D017173:Caenorhabditis elegans / Q000235:genetics / Q000378:metabolism / Q000502:physiology*; D029742:Caenorhabditis elegans Proteins; D015801:Helminth Proteins / Q000235:genetics; D007328:Insulin / Q000378:metabolism; D008136:Longevity / Q000235:genetics*; D019869:Phosphatidylinositol 3-Kinases; D011972:Receptor, Insulin / Q000235:genetics; D015398:Signal Transduction
D029742:Caenorhabditis elegans Proteins; D015801:Helminth Proteins; D007328:Insulin; D019869:Phosphatidylinositol 3-Kinases; C100662:AGE-1 protein, C elegans; C107483:DAF-2 protein, C elegans; D011972:Receptor, Insulin