Moseley B E
J Bacteriol. 1969 Feb;97(2):647-52. doi: 10.1128/jb.97.2.647-652.1969.
Various aspects of the repair of ultraviolet (UV) radiation-induced damage were compared in wild-type Micrococcus radiodurans and two UV-sensitive mutants. Unlike the wild type, the mutants are more sensitive to radiation at 265 nm than at 280 nm. The delay in deoxyribonucleic acid (DNA) synthesis following exposure to UV is about seven times as long in the mutants as in the wild type. All three strains excise UV-induced pyrimidine dimers from their DNA, although the rate at which cytosine-thymine dimers are excised is slower in the mutants. The three strains also mend the single-strand breaks that appear in the irradiated DNA as a result of dimer excision, although the process is less efficient in the mutants. It is suggested that the increased sensitivity of the mutants to UV radiation may be caused by a partial defect in the second step of dimer excision.
在野生型耐辐射微球菌和两个紫外线敏感突变体中,对紫外线(UV)辐射诱导损伤的修复的各个方面进行了比较。与野生型不同,这些突变体对265nm的辐射比280nm的辐射更敏感。暴露于紫外线后,突变体中脱氧核糖核酸(DNA)合成的延迟时间大约是野生型的七倍。所有这三种菌株都能从其DNA中切除紫外线诱导的嘧啶二聚体,尽管突变体中胞嘧啶 - 胸腺嘧啶二聚体的切除速率较慢。这三种菌株还能修复由于二聚体切除而在受辐照DNA中出现的单链断裂,尽管该过程在突变体中效率较低。有人认为,突变体对紫外线辐射敏感性增加可能是由于二聚体切除第二步中的部分缺陷所致。