Person S, McCloskey J A, Snipes W, Bockrath R C
Genetics. 1974 Dec;78(4):1035-49. doi: 10.1093/genetics/78.4.1035.
Ultraviolet mutagenesis and its repair were studied mainly in WU36-10-89, a uvr(-) strain of Escherichia coli containing a UAG mutation in a gene for leucine biosynthesis. Following ultraviolet (UV) irradiation revertants appearing with or without direct photoreactivation (PR) were classified according to the presence and type of suppressor they contained. We find UV mutation production to be quite specific. An analysis of revertants produced by UV indicates they are formed mainly from GC --> AT and that the miscoding is due to a cytosine residue at the site of mutation in a cytosine-thymine (CT) dimer. We propose that the dimer serves as template during some aspects of repair replication and at the time of replication the C in the dimer directs the insertion of A in the complementary strand. We also note that C --> A and T -->G changes caused by a CT dimer occur much less frequently.
紫外线诱变及其修复主要在大肠杆菌的uvr(-)菌株WU36 - 10 - 89中进行研究,该菌株在亮氨酸生物合成基因中存在UAG突变。紫外线(UV)照射后,出现的回复突变体无论有无直接光复活作用(PR),都根据其所含抑制子的存在情况和类型进行分类。我们发现紫外线诱变产生具有相当的特异性。对紫外线产生的回复突变体的分析表明,它们主要由GC→AT形成,错义编码是由于胞嘧啶 - 胸腺嘧啶(CT)二聚体中突变位点的胞嘧啶残基所致。我们提出,在修复复制的某些方面,二聚体充当模板,并且在复制时,二聚体中的C指导互补链中A的插入。我们还注意到,由CT二聚体引起的C→A和T→G变化发生的频率要低得多。