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http://purl.uniprot.org/citations/28557996http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/28557996http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/28557996http://www.w3.org/2000/01/rdf-schema#comment"Dietary restriction (DR) and reduced insulin growth factor (IGF) signaling extend lifespan in Caenorhabditis elegans and other eukaryotic organisms. Autophagy, an evolutionarily conserved lysosomal degradation pathway, has emerged as a central pathway regulated by various longevity signals including DR and IGF signaling in promoting longevity in a variety of eukaryotic organisms. However, the mechanism remains unclear. Here we show that the autophagy protein ATG-18 acts cell non-autonomously in neuronal and intestinal tissues to maintain C. elegans wildtype lifespan and to respond to DR and IGF-mediated longevity signaling. Moreover, ATG-18 activity in chemosensory neurons that are involved in food detection sufficiently mediates the effect of these longevity pathways. Additionally, ATG-18-mediated cell non-autonomous signaling depends on the release of neurotransmitters and neuropeptides. Interestingly, our data suggest that neuronal and intestinal ATG-18 acts in parallel and converges on unidentified neurons that secrete neuropeptides to regulate C. elegans lifespan through the transcription factor DAF-16/FOXO in response to reduced IGF signaling."xsd:string
http://purl.uniprot.org/citations/28557996http://purl.org/dc/terms/identifier"doi:10.1371/journal.pgen.1006764"xsd:string
http://purl.uniprot.org/citations/28557996http://purl.org/dc/terms/identifier"doi:10.1371/journal.pgen.1006764"xsd:string
http://purl.uniprot.org/citations/28557996http://purl.uniprot.org/core/author"Zhang J."xsd:string
http://purl.uniprot.org/citations/28557996http://purl.uniprot.org/core/author"Zhang J."xsd:string
http://purl.uniprot.org/citations/28557996http://purl.uniprot.org/core/author"Jia K."xsd:string
http://purl.uniprot.org/citations/28557996http://purl.uniprot.org/core/author"Jia K."xsd:string
http://purl.uniprot.org/citations/28557996http://purl.uniprot.org/core/author"Kaul T."xsd:string
http://purl.uniprot.org/citations/28557996http://purl.uniprot.org/core/author"Kaul T."xsd:string
http://purl.uniprot.org/citations/28557996http://purl.uniprot.org/core/author"Minnerly J."xsd:string
http://purl.uniprot.org/citations/28557996http://purl.uniprot.org/core/author"Minnerly J."xsd:string
http://purl.uniprot.org/citations/28557996http://purl.uniprot.org/core/author"Parker T."xsd:string
http://purl.uniprot.org/citations/28557996http://purl.uniprot.org/core/author"Parker T."xsd:string
http://purl.uniprot.org/citations/28557996http://purl.uniprot.org/core/date"2017"xsd:gYear
http://purl.uniprot.org/citations/28557996http://purl.uniprot.org/core/date"2017"xsd:gYear
http://purl.uniprot.org/citations/28557996http://purl.uniprot.org/core/name"PLoS Genet."xsd:string
http://purl.uniprot.org/citations/28557996http://purl.uniprot.org/core/name"PLoS Genet."xsd:string
http://purl.uniprot.org/citations/28557996http://purl.uniprot.org/core/pages"E1006764"xsd:string
http://purl.uniprot.org/citations/28557996http://purl.uniprot.org/core/pages"E1006764"xsd:string
http://purl.uniprot.org/citations/28557996http://purl.uniprot.org/core/title"The cell non-autonomous function of ATG-18 is essential for neuroendocrine regulation of Caenorhabditis elegans lifespan."xsd:string
http://purl.uniprot.org/citations/28557996http://purl.uniprot.org/core/title"The cell non-autonomous function of ATG-18 is essential for neuroendocrine regulation of Caenorhabditis elegans lifespan."xsd:string
http://purl.uniprot.org/citations/28557996http://purl.uniprot.org/core/volume"13"xsd:string
http://purl.uniprot.org/citations/28557996http://purl.uniprot.org/core/volume"13"xsd:string