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Apfeld J., Kenyon C. Regulation of lifespan by sensory perception in Caenorhabditis elegans. Nature. 402:1999;804-809. This paper shows that lifespan is increased in eleven mutants that are affected in nine genes, all of which disrupt ciliated sensory nerve endings. Life extension is largely blocked by mutation of daf-16, and the long life of daf-2 mutants is not further extended by cilium-structure defects, suggesting that environmental cues modulate IIS. Lifespan in cilium-structure mutants was further increased by germline ablation. Surprisingly, in daf-10 and osm-10 mutants, ablation of the whole gonad also further extended lifespan.
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tph1 encodes tryptophan hydroxylase, required for synthesis of serotonin. This paper describes the phenotype resulting from deletion of tph-1: reduced feeding and egg laying, high levels of stored lipid, an extended reproductive period, and some dauer larva arrest. Analysis of mutant interactions suggest that both IIS and TGF-β signalling are reduced by the absence of serotonin.
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Sze J.Y., Victor M., Loer C., Shi Y., Ruvkun G. Food and metabolic signalling defects in a Caenorhabditis elegans serotonin-synthesis mutant. Nature. 403:2000;560-564. tph1 encodes tryptophan hydroxylase, required for synthesis of serotonin. This paper describes the phenotype resulting from deletion of tph-1: reduced feeding and egg laying, high levels of stored lipid, an extended reproductive period, and some dauer larva arrest. Analysis of mutant interactions suggest that both IIS and TGF-β signalling are reduced by the absence of serotonin.
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The authors of this study investigate where IIS genes daf-2 and age-1 function to control larval development, intestinal lipid levels, and lifespan. To do this, daf-2 and age-1 were expressed from cell-specific promoters in an otherwise mutant background. Restoration of IIS in neurones, but not muscle or intestine, fully rescued the mutant phenotype; however, the lipid-storage defect was also rescued by muscle-specific expression.
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sod3 encodes a Mn superoxide dismutase. sod-3 mRNA levels are increased in dauer larvae, and daf-2 mutant adults, but barely detectable in wild-type or clk-1 mutant adults. Intriguingly, sod-3 mRNA levels are highest in clk-1 daf-2 double mutants. This work suggests that sod-3 is down-regulated by IIS.
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AFX FKHR and FKHRL1 are mammalian DAF-16 homologues. Here, tissue distribution of mRNAs is examined. Further, all four transcription factors are found to bind to a core sequence TTGTTTAC - the daf-16 family protein binding element, DBE. The promoter of the C. elegans sod-3 gene, which encodes a Mn SOD, was found to contain a DBE. Thus, sod-3 is likely to be regulated by daf-16 directly.
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The cloning and sequence of daf-12 is described. This gene is widely expressed in target tissues: in adults in the nervous system and somatic gonad, both of which play a role in regulation of adult longevity. Mutant lesions cluster in ligand- and DNA-binding domains, and correspond to distinct phenotypic classes.
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Lifespan is examined in four dwarf mutants with defects in the Inr insulin/IGF receptor gene - the equivalent of the worm daf-2 gene. Although three are short-lived, the fourth exhibits an 85% increase in mean adult lifespan in females. Activity of the corpora allata, the site of juvenile hormone synthesis, is greatly reduced. Ectopic application of methoprene, a juvenile hormone analogue, suppresses the Inr life extension. This suggests neuroendocrine regulation of ageing in Drosophila.
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