Nucleic Acids Research Advance Access published online on January 18, 2008
Nucleic Acids Research, doi:10.1093/nar/gkm1161
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Molecular biology |
Longevity and resistance to stress correlate with DNA repair capacity in Caenorhabditis elegans
1Department of Life Sciences, University of Ulsan 680-749, Korea and 2Laboratory of Molecular Gerontology, Gerontology Research Center, National Institute on Aging, National Institutes of Health, Baltimore, MD 21224, USA
*To whom correspondence should be addressed. Tel: +1 82 52 259 2359; Fax: +1 82 52 259 1694; Email: bbccahn{at}mail.ulsan.ac.kr
Received November 15, 2007. Revised December 13, 2007. Accepted December 13, 2007.
DNA repair is an important mechanism by which cells maintain genomic integrity. Decline in DNA repair capacity or defects in repair factors are thought to contribute to premature aging in mammals. The nematode Caenorhabditis elegans is a good model for studying longevity and DNA repair because of key advances in understanding the genetics of aging in this organism. Long-lived C. elegans mutants have been identified and shown to be resistant to oxidizing agents and UV irradiation, suggesting a genetically determined correlation between DNA repair capacity and life span. In this report, gene-specific DNA repair is compared in wild-type C. elegans and stress-resistant C. elegans mutants for the first time. DNA repair capacity is higher in long-lived C. elegans mutants than in wild-type animals. In addition, RNAi knockdown of the nucleotide excision repair gene xpa-1 increased sensitivity to UV and reduced the life span of long-lived C. elegans mutants. These findings support that DNA repair capacity correlates with longevity in C. elegans.