Nakayama H, Shiota S, Umezu K
Department of Microbiology, Faculty of Dentistry, Kyushu University, Fukuoku, Japan.
Mutat Res. 1992 Jan;273(1):43-8. doi: 10.1016/0921-8777(92)90048-8.
Unlike its phage T4 counterpart (also known as endonuclease V), Micrococcus luteus UV endonuclease (pyrimidine dimer DNA glycosylase/apurinic-apyrimidinic endonuclease) has suffered from lack of genetic evidence to implicate it in the promotion of UV survival of the cell, i.e., mutants with its deficiency are no more UV-sensitive than the wild type. On the assumption that the contribution of UV endonuclease is obscured by the presence of a homolog of Escherichia coli UvrABC endonuclease, which has recently been identified in this bacterium, survival studies were carried out in its absence. With 254-nm UV irradiation, which generates not only pyrimidine dimers but also 6-4 photoproducts as lethal lesions, a double mutant defective in both UV endonuclease and the Uvr homolog was shown to be more sensitive than a single mutant defective only in the latter, with a dose reduction factor of approximately 2 at the survival level of 37%. Furthermore, molecular photosensitization, which produces only pyrimidine dimers, revealed an even greater difference in sensitivity, the dose reduction factor being about 3.4. These results indicate that the contribution to cell survival of UV endonuclease, an enzyme specific for pyrimidine dimers, is manifest if the backup by the Uvr homolog is absent.
与噬菌体T4对应的酶（也称为核酸内切酶V）不同，藤黄微球菌紫外线核酸内切酶（嘧啶二聚体DNA糖基化酶/脱嘌呤-脱嘧啶核酸内切酶）一直缺乏基因证据来表明它对细胞紫外线存活具有促进作用，即其缺陷型突变体并不比野生型对紫外线更敏感。基于紫外线核酸内切酶的作用被大肠杆菌UvrABC核酸内切酶的同源物掩盖这一假设（最近在这种细菌中已鉴定出该同源物），研究人员在缺乏该同源物的情况下进行了存活研究。用254纳米的紫外线照射，这种照射不仅会产生嘧啶二聚体，还会产生6-4光产物作为致死损伤，结果表明，紫外线核酸内切酶和Uvr同源物双缺陷的双突变体比仅后者缺陷的单突变体更敏感，在37%的存活水平下剂量降低因子约为2。此外，仅产生嘧啶二聚体的分子光致敏显示出更大的敏感性差异，剂量降低因子约为3.4。这些结果表明，如果没有Uvr同源物的备用作用，对嘧啶二聚体具有特异性的紫外线核酸内切酶对细胞存活的贡献就会显现出来。
