Reduced repair of X-ray-induced DNA lesions in cells without functioning DNA polymerase alpha.
X irradiation of cells induces damage in the DNA, which can be detected as fragmentation of the DNA in alkali. To examine whether DNA polymerase alpha plays a role in the X-ray-induced fragmentation of the DNA, cells with and without functioning DNA polymerase alpha have been compared. We have used the drug aphidicolin, which is a specific inhibitor of polymerase alpha. The results show that DNA of aphidicolin-treated cells is more easily fragmented in alkali than DNA of untreated cells. This is paralleled by a lower repair replication in cells without functioning DNA polymerase alpha. Hence polymerase alpha is involved in the repair process of lesions induced by X irradiation.
D016590:Aphidicolin; D002460:Cell Line; D004247:DNA / Q000528:radiation effects*; D004257:DNA Polymerase II / Q000037:antagonists & inhibitors / Q000502:physiology*; D004260:DNA Repair; D004273:DNA, Neoplasm / Q000528:radiation effects; D004224:Diterpenes / Q000494:pharmacology; D006801:Humans; D066298:In Vitro Techniques; D008545:Melanoma / Q000201:enzymology; D011831:Radiation Genetics
D004273:DNA, Neoplasm; D004224:Diterpenes; D016590:Aphidicolin; D004247:DNA; D004257:DNA Polymerase II