Journal
SCIENCE
Volume 350, Issue 6266, Pages 1375-1378Publisher
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/science.aac9257
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Funding
- NIH [R01AG038518, K99AG045200, T32AG000057]
- Samsung Advanced Institute of Technology
- Samsung Electronics Co.
- American Federation for Aging Research Postdoctoral Fellowship
- University of Washington Healthy Aging and Longevity Research Institute
- M. J. Murdock Charitable Trust
- National Institute on Aging, NIH [R00AGA0033050]
- University of Washington Nathan Shock Center of Excellence in the Basic Biology of Aging (NIH) [P30AG013280]
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Stabilization of the hypoxia-inducible factor 1 (HIF-1) increases life span and health span in nematodes through an unknown mechanism. We report that neuronal stabilization of HIF-1 mediates these effects in Caenorhabditis elegans through a cell nonautonomous signal to the intestine, which results in activation of the xenobiotic detoxification enzyme flavin-containing monooxygenase-2 (FMO-2). This prolongevity signal requires the serotonin biosynthetic enzyme TPH-1 in neurons and the serotonin receptor SER-7 in the intestine. Intestinal FMO-2 is also activated by dietary restriction (DR) and is necessary for DR-mediated life-span extension, which suggests that this enzyme represents a point of convergence for two distinct longevity pathways. FMOs are conserved in eukaryotes and induced by multiple life span-extending interventions in mice, which suggests that these enzymes may play a critical role in promoting health and longevity across phyla.
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