Tomilin N V, Paveltchuk E B, Mosevitskaya T V
Eur J Biochem. 1976 Oct 1;69(1):265-72. doi: 10.1111/j.1432-1033.1976.tb10882.x.
The ultraviolet-endonuclease isolated from Micrococcul luteus, specific for pyrimidine dimers, is able to attack not only ultraviolet-irradiated DNA (leading to 3'OH-5'PO4 single-strand breaks) but also superhelical covalently-closed circular DNA of phage lambda damaged by heating at 70 degrees C, pH 5.93. The number of endonuclease-sensitive defects in the DNA corresponds to the number of alkalilabile bonds (apurinic sites) induced by heating. Competition between ultraviolet-induced lesions and apurinic sites for ultraviolet-endonuclease is demonstrated; the affinity of the enzyme for pyrimidine dimers is about three times that for apurinic sites. Both activities of the ultraviolet-endonuclease are inactivated at 50 degrees C at the same rate. The ultraviolet-endonuclease is able to reduce the infectious activity of depurinated lambda DNA towards Ca2+-treated uvr+ and uvr A Escherichia coli cells. It is concluded that both pyrimidine dimers and apurinic sites can be recognized by one and the same enzyme (the ultraviolet-endonuclease).
从藤黄微球菌中分离出的紫外线内切酶，对嘧啶二聚体具有特异性，它不仅能够攻击紫外线照射过的DNA（导致3'-OH-5'-PO4单链断裂），还能攻击在70摄氏度、pH值为5.93的条件下加热而受损的噬菌体λ的超螺旋共价闭合环状DNA。DNA中对该内切酶敏感的缺陷数量与加热诱导产生的碱不稳定键（脱嘌呤位点）数量相对应。实验证明了紫外线诱导损伤与脱嘌呤位点对紫外线内切酶存在竞争；该酶对嘧啶二聚体的亲和力约为对脱嘌呤位点的三倍。紫外线内切酶的两种活性在50摄氏度时以相同速率失活。紫外线内切酶能够降低脱嘌呤的λDNA对经Ca2+处理的uvr+和uvr A大肠杆菌细胞的感染活性。由此得出结论，嘧啶二聚体和脱嘌呤位点都能被同一种酶（紫外线内切酶）识别。
