Park I S, Park J K, Koh H Y, Park S D
Department of Zoology, College of Natural Sciences, Seoul National University, Republic of Korea.
Cell Biol Toxicol. 1991 Jan;7(1):49-58. doi: 10.1007/BF00121329.
DNA repair synthesis induced by methyl methanesulfonate in preconditioned HeLa cells in which DNA replicative synthesis had been highly suppressed was inhibited by aphidicolin (an inhibitor of DNA polymerases alpha and delta) and dideoxythymidine (ddThR, an inhibitor of DNA polymerase beta). Incomplete repair patches sensitive to exonuclease III were accumulated in the presence of aphidicolin while not in the presence of ddThR. These patches were comopleted by the combined action of Klenow fragment and T4 DNA ligase, indicating that the single-stranded gaps were formed during the repair synthesis. Moreover, ddThR had little effect on the repair synthesis in the presence of aphidicolin. Thus, the results suggest that the single-stranded gaps may be sealed first by aphidicolin-sensitive polymerase followed by ddThR-sensitive DNA polymerase on the same site of the repair patch.
甲磺酸甲酯在DNA复制性合成已被高度抑制的预处理HeLa细胞中诱导的DNA修复合成，受到阿非科林（一种DNA聚合酶α和δ的抑制剂）和双脱氧胸苷（ddThR，一种DNA聚合酶β的抑制剂）的抑制。在阿非科林存在的情况下，对核酸外切酶III敏感的不完全修复片段会积累，而在ddThR存在的情况下则不会。这些片段通过Klenow片段和T4 DNA连接酶的联合作用得以完成，这表明在修复合成过程中形成了单链缺口。此外，在阿非科林存在的情况下，ddThR对修复合成几乎没有影响。因此，结果表明单链缺口可能首先由对阿非科林敏感的聚合酶封闭，随后由对ddThR敏感的DNA聚合酶在修复片段的同一位点封闭。
