title: Elucidating the Mechanism of Weissella-dependent Lifespan Extension in Caenorhabditis elegans.
abstract: The mechanism whereby lactic acid bacteria extend the lifespan of Caenorhabditis elegans has previously been elucidated. However, the role of Weissella species has yet not been studied. We show that Weissella koreensis and Weissella cibaria significantly (p < 0.05) extend the lifespan of C. elegans compared with Escherichia coli OP50 and induce the expression of several genes related to lifespan extension (daf-16, aak-2, jnk-1, sod-3 and hif-1). Oral administration of Weissella altered reactive oxygen species (ROS) production and lowered the accumulation of lipofuscin and increased locomotor activity (which translates to a delay in ageing). Moreover, Weissella-fed C. elegans had decreased body sizes, brood sizes, ATP levels and pharyngeal pumping rates compared with E. coli OP50-fed worms. Furthermore, mutations in sod-3, hif-1 or skn-1 did not alter lifespan extension compared with wild-type C. elegans. However, C. elegans failed to display lifespan extension in loss-of-function mutants of daf-16, aak-2 and jnk-1, which highlights the potential role of these genes in Weissella-induced longevity in C. elegans. Weissella species extend C. elegans lifespan by activating DAF-16 via the c-Jun N-terminal kinase (JNK) pathway, which is related to stress response, and the AMP-activated protein kinase (AMPK)-pathway that is activated by dietary restriction.
authors.affiliation: Department of Public Health Science (Brain Korea 21 PLUS program), Graduate School, Korea University, Seoul 136-701, Republic of Korea.
authors.forename: Jiyun
authors.initials: J
authors.lastname: Lee
authors.affiliation: Department of Public Health Science (Brain Korea 21 PLUS program), Graduate School, Korea University, Seoul 136-701, Republic of Korea.
authors.forename: Gayeung
authors.initials: G
authors.lastname: Kwon
authors.affiliation: Department of Public Health Science (Brain Korea 21 PLUS program), Graduate School, Korea University, Seoul 136-701, Republic of Korea.|School of Biosystem and Biomedical Science, College of Health Science, Korea University, Seoul, Republic of Korea.|Department of Laboratory Medicine, Korea University Guro Hospital, Seoul, Republic of Korea.
authors.forename: Young-Hee
authors.initials: YH
authors.lastname: Lim
mesh_terms: D055372:AMP-Activated Protein Kinases / Q000378:metabolism; D000255:Adenosine Triphosphate / Q000378:metabolism; D000375:Aging; D000818:Animals; D015415:Biomarkers / Q000378:metabolism; D017173:Caenorhabditis elegans / Q000382:microbiology*; D029742:Caenorhabditis elegans Proteins / Q000235:genetics / Q000378:metabolism; D004926:Escherichia coli / Q000502:physiology; D005518:Food Preferences; D051858:Forkhead Transcription Factors / Q000378:metabolism; D048031:JNK Mitogen-Activated Protein Kinases / Q000378:metabolism; D008062:Lipofuscin / Q000378:metabolism; D008136:Longevity; D009043:Motor Activity; D009154:Mutation; D017382:Reactive Oxygen Species / Q000378:metabolism; D015398:Signal Transduction; D058836:Weissella / Q000502:physiology*
chemical_list: D015415:Biomarkers; D029742:Caenorhabditis elegans Proteins; D051858:Forkhead Transcription Factors; D008062:Lipofuscin; D017382:Reactive Oxygen Species; C108831:daf-16 protein, C elegans; D000255:Adenosine Triphosphate; D048031:JNK Mitogen-Activated Protein Kinases; D055372:AMP-Activated Protein Kinases