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.
Cowen
T
T
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
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