Open AccessDietary restriction suppresses proteotoxicity and enhances longevity by an hsf‐1 ‐dependent mechanism in Caenorhabditis elegans
Author(s) -
Steinkraus Katherine A.,
Smith Erica D.,
Davis Christina,
Carr Daniel,
Pendergrass William R.,
Sutphin George L.,
Kennedy Brian K.,
Kaeberlein Matt
Publication year - 2008
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 - 10.1111/j.1474-9726.2008.00385.x
Subject(s) - proteotoxicity , longevity , biology , evolvability , caenorhabditis elegans , mechanism (biology) , microbiology and biotechnology , disease , protein aggregation , genetics , medicine , gene , philosophy , epistemology
Summary Dietary restriction increases lifespan and slows the onset of age‐associated disease in organisms from yeast to mammals. In humans, several age‐related diseases are associated with aberrant protein folding or aggregation, including neurodegenerative disorders such as Alzheimer's, Parkinson's, and Huntington's diseases. We report here that dietary restriction dramatically suppresses age‐associated paralysis in three nematode models of proteotoxicity. Similar to its longevity‐enhancing properties, dietary restriction protects against proteotoxicity by a mechanism distinct from reduced insulin/IGF‐1‐like signaling. Instead, the heat shock transcription factor, hsf‐1 , is required for enhanced thermotolerance, suppression of proteotoxicity, and lifespan extension by dietary restriction. These findings demonstrate that dietary restriction confers a general protective effect against proteotoxicity and promotes longevity by a mechanism involving hsf‐1 .