Longevity and resistance to stress correlate with DNA repair capacity in Caenorhabditis elegans.
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.
Hyun
Moonjung
M
Department of Life Sciences, University of Ulsan 680-749, Korea.
Lee
Jihyun
J
Lee
Kyungjin
K
May
Alfred
A
Bohr
Vilhelm A
VA
Ahn
Byungchan
B
D000818:Animals; D017173:Caenorhabditis elegans / Q000235:genetics* / Q000254:growth & development / Q000528:radiation effects; D029742:Caenorhabditis elegans Proteins / Q000037:antagonists & inhibitors / Q000235:genetics; D004260:DNA Repair; D008136:Longevity / Q000235:genetics*; D009154:Mutation; D018384:Oxidative Stress; D011740:Pyrimidine Dimers / Q000378:metabolism; D034622:RNA Interference; D014466:Ultraviolet Rays
D029742:Caenorhabditis elegans Proteins; D011740:Pyrimidine Dimers