Excision repair of UV radiation-induced DNA damage in Caenorhabditis elegans.
Radioimmunoassays were used to monitor the removal of antibody-binding sites associated with the two major UV radiation-induced DNA photoproducts [cyclobutane dimers and (6-4) photoproducts]. Unlike with cultured human cells, where (6-4) photoproducts are removed more rapidly than cyclobutane dimers, the kinetics of repair were similar for both lesions. Repair capacity in wild type diminished throughout development. The radioimmunoassays were also employed to confirm the absence of photoreactivation in C. elegans. In addition, three radiation-sensitive mutants (rad-1, rad-2, rad-7) displayed normal repair capacities. An excision defect was much more pronounced in larvae than embryos in the fourth mutant tested (rad-3). This correlates with the hypersensitivity pattern of this mutant and suggests that DNA repair may be developmentally regulated in C. elegans. The mechanism of DNA repair in C. elegans as well as the relationship between the repair of specific photoproducts and UV radiation sensitivity during development are discussed.
Department of Biology, Texas Christian University, Fort Worth 76129.
P S
PS
Hartman
J
J
Hevelone
V
V
Dwarakanath
D L
DL
Mitchell
D000818:Animals; D002107:Caenorhabditis / Q000235:genetics / Q000254:growth & development / Q000378:metabolism*; D004247:DNA / Q000528:radiation effects; D004249:DNA Damage; D004260:DNA Repair; D007700:Kinetics; D007814:Larva / Q000378:metabolism / Q000528:radiation effects; D010777:Photochemistry; D011740:Pyrimidine Dimers / Q000378:metabolism; D011836:Radiation Tolerance; D014466:Ultraviolet Rays
D011740:Pyrimidine Dimers; D004247:DNA