Mullenders L H, van Kesteren A C, Bussmann C J, van Zeeland A A, Natarajan A T
Carcinogenesis. 1986 Jun;7(6):995-1002. doi: 10.1093/carcin/7.6.995.
The repair of u.v.-induced damage in human and rodent cells was investigated at the level of DNA loops attached to the nuclear matrix. After 2 h post-u.v. incubation, DNase I digestion studies revealed a 3- to 4-fold enrichment of repair-labeled DNA at the nuclear matrix in four xeroderma pigmentosum cell strains belonging to complementation group C. This non-random distribution was not affected by treatment with sodium butyrate. In other cells with limited excision repair, i.e. two xeroderma pigmentosum cell strains of complementation group D and Syrian hamster embryonic cells, as well as in HeLa cells and normal human fibroblasts, no enrichment of repair-labeled DNA at the nuclear matrix was observed. Visualization of repair events in DNA loops by autoradiography of DNA halo-matrix structures confirmed the biochemical observations. The presence or absence of preferential repair of nuclear matrix-associated DNA paralleled the presence or absence of inhomogeneity in the distribution of T4 endonuclease-V-sensitive sites. A detailed analysis of repair events in xeroderma pigmentosum cells of complementation group C showed that after 2 h post-u.v. incubation, repair events were found at both attachment sites in a limited number of loops and that large domains of loops were not subjected to repair.
在与核基质相连的DNA环水平上，研究了人类和啮齿动物细胞中紫外线诱导损伤的修复情况。紫外线照射后2小时，脱氧核糖核酸酶I消化研究显示，在属于互补组C的四种着色性干皮病细胞株中，核基质处修复标记的DNA富集了3至4倍。这种非随机分布不受丁酸钠处理的影响。在其他切除修复有限的细胞中，即互补组D的两种着色性干皮病细胞株和叙利亚仓鼠胚胎细胞，以及在HeLa细胞和正常人成纤维细胞中，未观察到核基质处修复标记的DNA富集。通过DNA晕环-基质结构的放射自显影对DNA环中的修复事件进行可视化，证实了生化观察结果。核基质相关DNA的优先修复的存在与否与T4内切核酸酶-V敏感位点分布的不均匀性的存在与否平行。对互补组C的着色性干皮病细胞中的修复事件进行的详细分析表明，紫外线照射后2小时，在有限数量的环的两个附着位点均发现了修复事件，并且大量的环区域未进行修复。
