{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Guerrero GA"],"funding":["German Research Foundation","European Research Council","Max-Planck-Gesellschaft"],"pagination":["e53174"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC8460253"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["10"],"pubmed_abstract":["Longevity is often associated with stress resistance, but whether they are causally linked is incompletely understood. Here we investigate chemosensory-defective Caenorhabditis elegans mutants that are long-lived and stress resistant. We find that mutants in the intraflagellar transport protein gene osm-3 were significantly protected from tunicamycin-induced ER stress. While osm-3 lifespan extension is dependent on the key longevity factor DAF-16/FOXO, tunicamycin resistance was not. osm-3 mutants are protected from bacterial pathogens, which is pmk-1 p38 MAP kinase dependent, while TM resistance was pmk-1 independent. Expression of P-glycoprotein (PGP) xenobiotic detoxification genes was elevated in osm-3 mutants and their knockdown or inhibition with verapamil suppressed tunicamycin resi"],"journal":["eLife"],"pubmed_title":["NHR-8 and P-glycoproteins uncouple xenobiotic resistance from longevity in chemosensory C. elegans mutants."],"pmcid":["PMC8460253"],"funding_grant_id":["73111208","640254","ERC-StG 640254","SFB 829"],"pubmed_authors":["Hartman MD","Schilling K","Alonso-De Gennaro MJ","Guerrero GA","Benayoun BA","Denzel MS","Derisbourg MJ","Wester LE","Dinort JE","Lu RJ","Mayr FA","Giorda M"],"additional_accession":[]},"is_claimable":false,"name":"NHR-8 and P-glycoproteins uncouple xenobiotic resistance from longevity in chemosensory C. elegans mutants.","description":"Longevity is often associated with stress resistance, but whether they are causally linked is incompletely understood. Here we investigate chemosensory-defective Caenorhabditis elegans mutants that are long-lived and stress resistant. We find that mutants in the intraflagellar transport protein gene osm-3 were significantly protected from tunicamycin-induced ER stress. While osm-3 lifespan extension is dependent on the key longevity factor DAF-16/FOXO, tunicamycin resistance was not. osm-3 mutants are protected from bacterial pathogens, which is pmk-1 p38 MAP kinase dependent, while TM resistance was pmk-1 independent. Expression of P-glycoprotein (PGP) xenobiotic detoxification genes was elevated in osm-3 mutants and their knockdown or inhibition with verapamil suppressed tunicamycin resi","dates":{"release":"2021-01-01T00:00:00Z","publication":"2021 Aug","modification":"2025-04-19T06:08:29.06Z","creation":"2022-02-11T13:38:21.33Z"},"accession":"S-EPMC8460253","cross_references":{"pubmed":["34448454"],"doi":["10.7554/eLife.53174"]}}