{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Zheng T"],"funding":["University of Michigan","National Natural Science Foundation of China"],"pagination":["105266"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC9593246"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["25(11)"],"pubmed_abstract":["Reducing the rate of translation promotes longevity in multiple organisms, representing a conserved mechanism for lifespan extension. Aminoacyl-tRNA synthetases (ARSs) catalyze the loading of amino acids to their cognate tRNAs, thereby playing an essential role in translation. Mutations in ARS genes are associated with various human diseases. However, little is known about the role of ARSs in aging, particularly whether and how these genes regulate lifespan. Here, using <i>Caenorhabditis elegans</i> as a model, we systematically characterized the role of all three types of ARS genes in lifespan regulation, including mitochondrial, cytoplasmic, and cyto-mito bifunctional ARS genes. We found that, as expected, RNAi knockdown of mitochondrial ARS genes extended lifespan. Surprisingly, knockin"],"journal":["iScience"],"pubmed_title":["Cytoplasmic and mitochondrial aminoacyl-tRNA synthetases differentially regulate lifespan in <i>Caenorhabditis elegans</i>."],"pmcid":["PMC9593246"],"funding_grant_id":["81872945","32171146","81720108031"],"pubmed_authors":["Luo Q","Liu J","Xu XZS","Han C","Gong J","Zheng T","Zhou J","Chun L"],"additional_accession":[]},"is_claimable":false,"name":"Cytoplasmic and mitochondrial aminoacyl-tRNA synthetases differentially regulate lifespan in <i>Caenorhabditis elegans</i>.","description":"Reducing the rate of translation promotes longevity in multiple organisms, representing a conserved mechanism for lifespan extension. Aminoacyl-tRNA synthetases (ARSs) catalyze the loading of amino acids to their cognate tRNAs, thereby playing an essential role in translation. Mutations in ARS genes are associated with various human diseases. However, little is known about the role of ARSs in aging, particularly whether and how these genes regulate lifespan. Here, using <i>Caenorhabditis elegans</i> as a model, we systematically characterized the role of all three types of ARS genes in lifespan regulation, including mitochondrial, cytoplasmic, and cyto-mito bifunctional ARS genes. We found that, as expected, RNAi knockdown of mitochondrial ARS genes extended lifespan. Surprisingly, knockin","dates":{"release":"2022-01-01T00:00:00Z","publication":"2022 Nov","modification":"2026-07-14T17:28:48.111Z","creation":"2025-04-04T23:19:32.966Z"},"accession":"S-EPMC9593246","cross_references":{"pubmed":["36304099"],"doi":["10.1016/j.isci.2022.105266"]}}