Tomilin N V, Mosevitskaya T V
Mutat Res. 1975 Feb;27(2):147-56. doi: 10.1016/0027-5107(75)90074-3.
UV-endonuclease from Microcossuc luteus induces single-stranded breaks in UV-irradiated DNA of phage lambda and the average length of the fragments produced (after UV-doses to DNA of 135 and 675 erg/mm2) is equal to the average spacing between pyrimidine dimers. The plaque-forming ability of UV-irradiated lambda DNA used to infect Ca++-treated uvr A6, uvrB5 or uvrC34 recipient Escherichia coli cells (but not uve+ cells) may be significantly enhanced by treatment of lambda DNA with UV-endonuclease. This enzyme strongly decreases the reactivation of UV-irradiated lambda DNA caused by UV-irradiation of uvr+ or uvrA6 Ca++-treated cells and eliminates most clear-mutations especially if mutations are analysed using Ca++-treated uvr A6 recipient cells. It is concluded that UV-endonuclease switches a significant part of potentially mutagenic pyrimidine dimers from the UV-induced "error-prone" repair pathway to "error-free" excision repair pathway.
来自藤黄微球菌的紫外线内切酶可在噬菌体λ经紫外线照射的DNA中诱导产生单链断裂,并且(在对DNA施加135和675尔格/平方毫米的紫外线剂量后)所产生片段的平均长度与嘧啶二聚体之间的平均间距相等。用于感染经Ca++处理的uvr A6、uvrB5或uvrC34受体大肠杆菌细胞(但不是uvr+细胞)的经紫外线照射的λDNA的噬菌斑形成能力,可通过用紫外线内切酶处理λDNA而得到显著增强。这种酶强烈降低由uvr+或uvrA6经Ca++处理的细胞的紫外线照射所引起的经紫外线照射的λDNA的复活,并消除大多数明显的突变,特别是当使用经Ca++处理的uvr A6受体细胞分析突变时。得出的结论是,紫外线内切酶将相当一部分潜在诱变的嘧啶二聚体从紫外线诱导的“易错”修复途径转换到“无错”切除修复途径。