Regulation of C. elegans Life-Span by Insulinlike Signaling in the Nervous System
pmid: 11021802
Regulation of C. elegans Life-Span by Insulinlike Signaling in the Nervous System
An insulinlike signaling pathway controls Caenorhabditis elegans aging, metabolism, and development. Mutations in the daf-2 insulin receptor–like gene or the downstream age-1 phosphoinositide 3-kinase gene extend adult life-span by two- to threefold. To identify tissues where this pathway regulates aging and metabolism, we restored daf-2 pathway signaling to only neurons, muscle, or intestine. Insulinlike signaling in neurons alone was sufficient to specify wild-type life-span, but muscle or intestinal signaling was not. However, restoring daf-2 pathway signaling to muscle rescued metabolic defects, thus decoupling regulation of life-span and metabolism. These findings point to the nervous system as a central regulator of animal longevity.
- Nagoya University Japan
- Harvard University United States
Neurons, Aging, Muscles, Recombinant Fusion Proteins, Longevity, Helminth Proteins, Catalase, Receptor, Insulin, Intestines, Phosphatidylinositol 3-Kinases, Phenotype, Gene Expression Regulation, Larva, Animals, Nervous System Physiological Phenomena, Caenorhabditis elegans, Caenorhabditis elegans Proteins, Promoter Regions, Genetic, Genes, Helminth, Signal Transduction
Neurons, Aging, Muscles, Recombinant Fusion Proteins, Longevity, Helminth Proteins, Catalase, Receptor, Insulin, Intestines, Phosphatidylinositol 3-Kinases, Phenotype, Gene Expression Regulation, Larva, Animals, Nervous System Physiological Phenomena, Caenorhabditis elegans, Caenorhabditis elegans Proteins, Promoter Regions, Genetic, Genes, Helminth, Signal Transduction
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