Variable pathogenicity determines individual lifespan in Caenorhabditis elegans

• Published in: PLoS genetics Vol. 7; no. 4; p. e1002047
• Main Authors: Sánchez-Blanco, Adolfo, Kim, Stuart K
• Format: Journal Article
• Language: English
• Published: United States Public Library of Science 01.04.2011; Public Library of Science (PLoS)
• Subjects: Age; Aging; Aging - genetics; Animals; Animals, Genetically Modified - genetics; Animals, Genetically Modified - growth & development; Animals, Genetically Modified - metabolism; Bacillus subtilis - pathogenicity; Biology; Caenorhabditis elegans; Caenorhabditis elegans - genetics; Caenorhabditis elegans - growth & development; Caenorhabditis elegans - microbiology; Caenorhabditis elegans Proteins - genetics; Caenorhabditis elegans Proteins - metabolism; Cloning; E coli; Escherichia coli - pathogenicity; Food; Gene Expression; Genes, Reporter; Genetic aspects; Genetics; Green Fluorescent Proteins - metabolism; Longevity; Microbiology; Physiological aspects; Superoxide Dismutase - genetics; Superoxide Dismutase - metabolism; United States
• ISSN: 1553-7404; 1553-7390; 1553-7404
• DOI: 10.1371/journal.pgen.1002047

A common property of aging in all animals is that chronologically and genetically identical individuals age at different rates. To unveil mechanisms that influence aging variability, we identified markers of remaining lifespan for Caenorhabditis elegans. In transgenic lines, we expressed fluorescent reporter constructs from promoters of C. elegans genes whose expression change with age. The expression levels of aging markers in individual worms from a young synchronous population correlated with their remaining lifespan. We identified eight aging markers, with the superoxide dismutase gene sod-3 expression being the best single predictor of remaining lifespan. Correlation with remaining lifespan became stronger if expression from two aging markers was monitored simultaneously, accounting for up to 49% of the variation in individual lifespan. Visualizing the physiological age of chronologically-identical individuals allowed us to show that a major source of lifespan variability is different pathogenicity from individual to individual and that the mechanism involves variable activation of the insulin-signaling pathway.