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- W3201099487 abstract "Insulin/IGF-1 signaling (IIS) regulates various physiological aspects in numerous species. In Caenorhabditis elegans, mutations in the daf-2/insulin/IGF-1 receptor dramatically increase lifespan and immunity, but generally impair motility, growth, and reproduction. Whether these pleiotropic effects can be dissociated at a specific step in insulin/IGF-1 signaling pathway remains unknown. Through performing a mutagenesis screen, we identified a missense mutation daf-18(yh1) that alters a cysteine to tyrosine in DAF-18/PTEN phosphatase, which maintained the long lifespan and enhanced immunity, while improving the reduced motility in adult daf-2 mutants. We showed that the daf-18(yh1) mutation decreased the lipid phosphatase activity of DAF-18/PTEN, while retaining a partial protein tyrosine phosphatase activity. We found that daf-18(yh1) maintained the partial activity of DAF-16/FOXO but restricted the detrimental upregulation of SKN-1/NRF2, contributing to beneficial physiological traits in daf-2 mutants. Our work provides important insights into how one evolutionarily conserved component, PTEN, can coordinate animal health and longevity." @default.
- W3201099487 created "2021-09-27" @default.
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- W3201099487 date "2021-09-24" @default.
- W3201099487 modified "2023-10-10" @default.
- W3201099487 title "A PTEN variant uncouples longevity from impaired fitness in Caenorhabditis elegans with reduced insulin/IGF-1 signaling" @default.
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- W3201099487 doi "https://doi.org/10.1038/s41467-021-25920-w" @default.
- W3201099487 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/8463539" @default.
- W3201099487 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/34561453" @default.
- W3201099487 hasPublicationYear "2021" @default.
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