THE INDUCTION OF THYMINE DIMERS IN ULTRAVIOLET-IRRADIATED MAMMALIAN CELLS.
THE INDUCTION OF THYMINE DIMERS IN ULTRAVIOLET-IRRADIATED MAMMALIAN CELLS.
复制标题
紫外线照射的哺乳动物细胞中胸腺嘧啶二聚体的诱导。
DOI：
10.2307/3571885
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发表时间：
1965
影响因子：
3.4
通讯作者：
W. Carrier
中科院分区：
文献类型：
--
作者：
J. Trosko;E. Chu;W. Carrier
众所周知，基因突变和染色体畸变都可以由紫外线引起（见综述：1）。突变的作用谱与核酸吸收有关(2)，紫外线诱导的Tradescantia花粉粒染色体畸变的作用谱与核酸吸收谱大致相似(3)。同样，哺乳动物细胞中紫外线诱导的染色体畸变频率随波长而变化，并在2650 a左右达到峰值(4)。实验进一步证明，用5-溴脱氧尿嘧啶或5-碘脱氧尿嘧啶代替胸腺嘧啶可大大提高诱导哺乳动物染色体断裂的紫外线敏感性。这些结果表明，DNA是导致染色体畸变的紫外线损伤的主要目标(4)。紫外线对核酸及其成分的影响已成为许多研究的主题（见综述：5,6）。紫外线对DNA的损伤包括光水合作用、交联作用和胸腺嘧啶二聚体的形成。特别是，最近的研究表明，胸腺嘧啶二聚化可能在紫外线诱导的转化活性损伤中占很大比例(7)，也可能是细菌中DNA合成能力丧失的主要原因（8,9）。已经发现转化原理的光活化可以用二聚体分裂来解释(7)。此外，在某些大肠杆菌菌株中，紫外线诱导的胸腺嘧啶二聚体，连同一些邻近的核苷酸，可以通过似乎是黑暗修复过程被切除（10,11）。如果染色体DNA是导致染色体断裂的紫外线损伤位点的结论是正确的，那么确定导致染色体断裂的诱导分子改变的性质是有意义的。本报告介绍
It is well established that both gene mutations and chromosome aberrations can be induced by ultraviolet (UV) light (see review: 1). The action spectrum for mutation implicates nucleic acid absorption (2), and the action spectrum for the UVinduced chromosome aberrations in Tradescantia pollen grains approximately parallels the absorption spectrum of nucleic acids (3). Similarly, the frequency of UVinduced chromosome aberrations in mammalian cells varies with wavelength and reaches a peak around 2650 A (4). It has been further demonstrated that substitution of thymidine by 5-bromodeoxyuridine or 5-iododeoxyuridine greatly enhances the UV-sensitivity in the induction of mammalian chromosome breaks. These results suggest that DNA is the primary target of the UV injury that leads to chromosome aberrations (4). The effects of UV on nucleic acids and their constituents have been the subject of numerous investigations (see reviews: 5, 6). The kinds of UV damage to DNA include photohydration, cross-linkage, and the formation of thymine dimer. In particular, recent work has indicated that thymine dimerization may account for a large proportion of the UV-induced damage to transforming activity (7) and probably for much of the loss of DNA synthetic capacity in bacteria (8, 9). It has been found that the photoreactivation of transforming principle can be accounted for by dimer splitting (7). Furthermore, in certain strains of Escherichia coli, UV-induced thymine dimers, together with a few neighboring nucleotides, can be excised by what seems to be a dark repair process (10, 11). If the conclusion is correct that chromosomal DNA is the site of UV injury that leads to chromosome breaks, it is of interest to determine the nature of the induced molecular alteration(s) responsible for chromosome breaks. This report presents