Keyse S M, Tyrrell R M
Mutat Res. 1985 Jul;146(1):109-19. doi: 10.1016/0167-8817(85)90061-6.
We have characterised far-ultraviolet-radiation-induced DNA-repair synthesis in permeabilised arrested (non-dividing) primary human skin fibroblasts. Approximately half the maximum repair synthesis is seen after a UV fluence of 4.0 Jm-2 and little additional incorporation was observed at fluences above 20.0 Jm-2. UV-damaged permeable cells were treated with specific inhibitors of DNA polymerase alpha and beta, both alone and in combination. The degree of inhibition of repair incorporation by aphidicolin indicates that polymerase alpha is involved in the majority (85-90%) of repair synthesis after both high and low (less than 4.0 Jm-2) UV fluences. Dideoxythymidine triphosphate seems able to inhibit DNA-repair synthesis only when polymerase alpha is fully or almost fully functional, indicating that polymerase beta is unable to substitute in repair for an alpha polymerase blocked by aphidicolin. These data suggest that the two enzymes may act sequentially to complete repair patches rather than acting independently.
我们已经对经通透处理的静止（不分裂）原代人皮肤成纤维细胞中远紫外线辐射诱导的DNA修复合成进行了表征。在紫外线通量为4.0 Jm-2后，可观察到约一半的最大修复合成，而在通量高于20.0 Jm-2时，未观察到额外的掺入。对紫外线损伤的可渗透细胞单独或联合使用DNA聚合酶α和β的特异性抑制剂进行处理。阿非科林对修复掺入的抑制程度表明，在高和低（小于4.0 Jm-2）紫外线通量后，聚合酶α参与了大部分（85-90%）的修复合成。双脱氧胸苷三磷酸似乎仅在聚合酶α完全或几乎完全发挥功能时才能抑制DNA修复合成，这表明聚合酶β无法替代被阿非科林阻断的α聚合酶进行修复。这些数据表明，这两种酶可能依次作用以完成修复片段，而不是独立发挥作用。
