{"doi":"10.1038/nn1140","publisher":"Springer Nature","year":"2003","type":"journal_article","citation":{"ista":"Rogers C, Reale V, Kim K, Chatwin H, Li C, Evans P, de Bono M. 2003. Inhibition of Caenorhabditis elegans social feeding by FMRFamide-related peptide activation of NPR-1. Nature Neuroscience. 6(11), 1178–1185.","mla":"Rogers, Candida, et al. “Inhibition of Caenorhabditis Elegans Social Feeding by FMRFamide-Related Peptide Activation of NPR-1.” Nature Neuroscience, vol. 6, no. 11, Springer Nature, 2003, pp. 1178–85, doi:10.1038/nn1140.","ama":"Rogers C, Reale V, Kim K, et al. Inhibition of Caenorhabditis elegans social feeding by FMRFamide-related peptide activation of NPR-1. Nature Neuroscience. 2003;6(11):1178-1185. doi:10.1038/nn1140","ieee":"C. Rogers et al., “Inhibition of Caenorhabditis elegans social feeding by FMRFamide-related peptide activation of NPR-1,” Nature Neuroscience, vol. 6, no. 11. Springer Nature, pp. 1178–1185, 2003.","chicago":"Rogers, Candida, Vincenzina Reale, Kyuhyung Kim, Heather Chatwin, Chris Li, Peter Evans, and Mario de Bono. “Inhibition of Caenorhabditis Elegans Social Feeding by FMRFamide-Related Peptide Activation of NPR-1.” Nature Neuroscience. Springer Nature, 2003. https://doi.org/10.1038/nn1140.","short":"C. Rogers, V. Reale, K. Kim, H. Chatwin, C. Li, P. Evans, M. de Bono, Nature Neuroscience 6 (2003) 1178–1185.","apa":"Rogers, C., Reale, V., Kim, K., Chatwin, H., Li, C., Evans, P., & de Bono, M. (2003). Inhibition of Caenorhabditis elegans social feeding by FMRFamide-related peptide activation of NPR-1. Nature Neuroscience. Springer Nature. https://doi.org/10.1038/nn1140"},"issue":"11","publication_status":"published","_id":"6156","day":"12","status":"public","intvolume":" 6","language":[{"iso":"eng"}],"oa_version":"None","title":"Inhibition of Caenorhabditis elegans social feeding by FMRFamide-related peptide activation of NPR-1","quality_controlled":"1","author":[{"first_name":"Candida","full_name":"Rogers, Candida","last_name":"Rogers"},{"last_name":"Reale","full_name":"Reale, Vincenzina","first_name":"Vincenzina"},{"full_name":"Kim, Kyuhyung","first_name":"Kyuhyung","last_name":"Kim"},{"last_name":"Chatwin","full_name":"Chatwin, Heather","first_name":"Heather"},{"full_name":"Li, Chris","first_name":"Chris","last_name":"Li"},{"last_name":"Evans","full_name":"Evans, Peter","first_name":"Peter"},{"id":"4E3FF80E-F248-11E8-B48F-1D18A9856A87","last_name":"de Bono","full_name":"de Bono, Mario","first_name":"Mario","orcid":"0000-0001-8347-0443"}],"abstract":[{"text":"Social and solitary feeding in natural Caenorhabditis elegans isolates are associated with two alleles of the orphan G-protein-coupled receptor (GPCR) NPR-1: social feeders contain NPR-1 215F, whereas solitary feeders contain NPR-1 215V. Here we identify FMRFamide-related neuropeptides (FaRPs) encoded by the flp-18 and flp-21 genes as NPR-1 ligands and show that these peptides can differentially activate the NPR-1 215F and NPR-1 215V receptors. Multicopy overexpression of flp-21 transformed wild social animals into solitary feeders. Conversely, a flp-21 deletion partially phenocopied the npr-1(null) phenotype, which is consistent with NPR-1 activation by FLP-21 in vivo but also implicates other ligands for NPR-1. Phylogenetic studies indicate that the dominant npr-1 215V allele likely arose from an ancestral npr-1 215F gene in C. elegans. Our data suggest a model in which solitary feeding evolved in an ancestral social strain of C. elegans by a gain-of-function mutation that modified the response of NPR-1 to FLP-18 and FLP-21 ligands.","lang":"eng"}],"publication":"Nature Neuroscience","month":"10","date_published":"2003-10-12T00:00:00Z","volume":6,"pmid":1,"page":"1178-1185","user_id":"3E5EF7F0-F248-11E8-B48F-1D18A9856A87","publication_identifier":{"issn":["1097-6256","1546-1726"]},"date_updated":"2021-01-12T08:06:25Z","external_id":{"pmid":["14555955"]},"extern":"1","date_created":"2019-03-21T09:47:53Z"}