紫外线诱导突变的机制：大肠杆菌DNA聚合酶I复制的紫外线照射的聚（dC）的编码特性。
Mechanism of ultraviolet-induced mutagenesis: the coding properties of ultraviolet-irradiated poly(dC) replicated by E. coli DNA polymerase I.
作者信息
Lecomte P, Boiteux S, Doubleday O
出版信息
Nucleic Acids Res. 1981 Jul 24;9(14):3491-501. doi: 10.1093/nar/9.14.3491.
Abstract
We have identified three lesions rather than cyclobutane dimers which alter the properties of UV-irradiated poly(dC) as a template for E.coli DNA polymerase I, and have characterised these lesions with respect to their coding properties, rates of formation and decay, and their sensitivity to uracil DNA glycosylase. Our results lead us to conclude that these lesions are (1) cytosine hydrates, which code for cytosine and to a lesser extent thymine, (2) uracil hydrates, which code for adenine and are not sensitive to uracil DNA glycosylase, and (3) uracils, which code for adenine and are removed by uracil DNA glycosylase.
摘要
我们已鉴定出三种而非环丁烷二聚体的损伤，这些损伤改变了紫外线照射的聚（dC）作为大肠杆菌DNA聚合酶I模板的性质，并根据其编码特性、形成和衰变速率以及对尿嘧啶DNA糖基化酶的敏感性对这些损伤进行了表征。我们的结果使我们得出结论，这些损伤为：（1）胞嘧啶水合物，编码胞嘧啶，在较小程度上编码胸腺嘧啶；（2）尿嘧啶水合物，编码腺嘌呤，且对尿嘧啶DNA糖基化酶不敏感；（3）尿嘧啶，编码腺嘌呤，并可被尿嘧啶DNA糖基化酶去除。
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