Minderhout L, Grimbergen J, de Groot B
Mutat Res. 1978 Dec;52(3):313-22. doi: 10.1016/0027-5107(78)90170-7.
Non-essential bacteriophage T4 mutants uvs58 and uvs79 showed a lower UV sensitivity than either the excision-repair mutant v am5 or the replication-dependent recombination-repair mutant y10. The UV sensitivity of double and triple mutants carrying one of the mutations uvs58 or uvs79, and v am 5 or (and) y10 was higher than the sum of the sensitivities of the single mutants. The uvs58 mutation was mapped to the early gene region, close to amN81 (gene 41). The unirradiated mutants uvs58 and uvs79 accumulated newly synthesized DNA at a slower rate than wild-type T4. Double mutants uvs58:am59 and uvs79:am59 showed DNA synthesis in E. coli B su- to be arrested at a 3--5 times lower level than that in am59-infected cells. Chloramphenicol, added 9--12 min after infection, suppressed arrests of DNA synthesis, the double mutants showing a lag of 8 min as compared with am59. Results from analysis of sucrose gradients of parental uvs58 and uvs79 DNA were in agreement with the suggestion of a mutation in an early function. The mutants uvs58 and uvs79 are suggested to be defective in a component of the DNA replication apparatus with a function in the adaptation to irregularities in the DNA structure. The third pathway of UV repair is tentatively designated as non-catalytic replication repair.
非必需噬菌体T4突变体uvs58和uvs79对紫外线的敏感性低于切除修复突变体v am5或复制依赖性重组修复突变体y10。携带uvs58或uvs79其中一个突变以及v am5或(和)y10的双突变体和三突变体对紫外线的敏感性高于单突变体敏感性之和。uvs58突变被定位到早期基因区域,靠近amN81(基因41)。未受辐照的突变体uvs58和uvs79积累新合成DNA的速度比野生型T4慢。双突变体uvs58:am59和uvs79:am59在大肠杆菌B su-中的DNA合成停滞水平比感染am59的细胞低3至5倍。感染后9至12分钟添加氯霉素可抑制DNA合成的停滞,与am59相比,双突变体表现出8分钟的延迟。对亲本uvs58和uvs79 DNA的蔗糖梯度分析结果与早期功能发生突变的推测一致。推测突变体uvs58和uvs79在DNA复制装置的一个组分中存在缺陷,该组分在适应DNA结构不规则方面发挥作用。紫外线修复的第三条途径暂定为非催化复制修复。