The insulin/insulin-like growth factor-I signaling (IIS) pathway regulates larval diapause and adult lifespan in Caenorhabditis elegans. To date, many of the 38 insulin-like genes have been identified1), and a few of the genes have been investigated to identify their physiological function by RNAi knockdown. For instance, Murphy and co-workers reported that
ins-7 RNAi knockdown induces larva diapause and an extended lifespan.2) In our previous study, we disrupted Ceinsulin-1 (
ins-18) and Ceinsulin-2 (
ins-17), and elucidated their function on larval diapause and adult lifespan. Disruption of
ins-17 and/or
ins-18 reduced dauer larva formation caused by a crude extract of dauer-inducing pheromone, while the disruption showed no effect on adult lifespan. To investigate redundant function of the insulin-like genes, we disrupted the
ins-7, and then established multiple-gene-disrupted animals. Disruption of
ins-7 induced an extended lifespan as expected. Disruption of
ins-7 and
ins-17 also revealed lifespan extension, suggesting that
ins-17 is not relevant to lifespan regulation. On the other hand, disruption of
ins-7 and
ins-18 revealed no lifespan extension, indicating that
ins-18 is necessary for lifespan extension induced by the gene-disruption of
ins-7. Now we are measuring lifespan of each gene-disrupted animal under
daf-2(-) conditions. 1) Pierce, S. B. et al. (2001) Genes Dev. 15:672. 2) Murphy, C. T. et al. (2003) Nature 424:277.