Open AccessLifespan extension in C. elegans by a molecular chaperone dependent upon insulin‐like signals
Author(s) -
Walker Glenda A.,
Lithgow Gordon J.
Publication year - 2003
Publication title -
aging cell
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.103
H-Index - 140
eISSN - 1474-9726
pISSN - 1474-9718
DOI - 10.1046/j.1474-9728.2003.00045.x
Subject(s) - biology , caenorhabditis elegans , longevity , heat shock protein , gene , transcription factor , microbiology and biotechnology , mutant , genetics , chaperone (clinical) , insulin receptor , insulin , heat shock factor , phenotype , signalling , hsp70 , insulin resistance , endocrinology , medicine , pathology
Summary Insulin‐like signalling is a key determinate of lifespan in diverse species including mammals but the mechanism by which this pathway influences the rate of aging is unknown. In the roundworm Caenorhabditis elegans , mutations in the insulin‐like signalling pathway extend adult lifespan and are associated with up‐regulation of stress response genes including those for heat shock proteins (HSPs). We tested the hypothesis that the C. elegans insulin‐like signalling pathway determines longevity through modulating HSP levels. We introduced extra copies of the gene encoding HSP‐16 and this conferred stress resistance and longevity both in a wildtype and a long‐lived mutant strain. The DAF‐16 transcription factor is essential for maximal hsp‐16 expression and for lifespan extension conferred by hsp‐16 . This demonstrates that lifespan is determined in part by insulin‐like regulation of molecular chaperones.