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Resources » Paper

Kenji Gouda et al. (2007) International Worm Meeting "Redundant function of Caenorhabditis elegans insulin-like genes in larval diapause and adult lifespan."

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  • Comments on Kenji Gouda et al. (2007) International Worm Meeting "Redundant function of Caenorhabditis elegans insulin-like genes in larval diapause and adult lifespan." (0)

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    Publication type:
    Meeting_abstract
    WormBase ID:
    WBPaper00030010

    Kenji Gouda, Yohei Matsunaga, Yasuo Kimura, Keiko Gengyo-Ando, Shohei MItani, & Tsuyoshi Kawano (2007). Redundant function of Caenorhabditis elegans insulin-like genes in larval diapause and adult lifespan presented in International Worm Meeting. Unpublished information; cite only with author permission.

    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.


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