Lawrence C W, Gibbs P E, Borden A, Horsfall M J, Kilbey B J
Department of Biophysics, University of Rochester School of Medicine and Dentistry, NY 14642.
Mutat Res. 1993 May;299(3-4):157-63. doi: 10.1016/0165-1218(93)90093-s.
Data from experiments with single-stranded vectors that carry a site-specific cyclobutane dimer, pyrimidine (6-4) pyrimidone adduct, or abasic lesion, replicated in either E. coli or, in some cases, bakers' yeast, Saccharomyces cerevisiae, are used to examine two questions: (i) what factors are responsible for the lesion's mutagenicity? and (ii) what are the relative contributions of different photoproducts to the spectrum of UV-induced mutations? With respect to the first question, we suggest that the structure of the mutagen-modified template itself largely determines the kinds of mutations induced, but the relative frequencies of these mutations, the error frequency, and the bypass frequency are strongly dependent on the particular organism studied. With respect to the second question, we suggest that cyclobutane dimers may be responsible for most of the mutations in slowly replicating genomes because of the deamination of cytosine, and that the T-T, and to a lesser extent the T-C, (6-4) adducts play a greater role in the UV mutagenesis of quickly replicating viruses, such as M13 and lambda phage.
使用携带位点特异性环丁烷二聚体、嘧啶（6-4）嘧啶酮加合物或无碱基损伤的单链载体进行实验的数据，这些实验在大肠杆菌中进行复制，在某些情况下也在面包酵母酿酒酵母中进行，以研究两个问题：（i）哪些因素导致损伤的致突变性？（ii）不同光产物对紫外线诱导突变谱的相对贡献是什么？关于第一个问题，我们认为诱变剂修饰模板本身的结构在很大程度上决定了诱导的突变类型，但这些突变的相对频率、错误频率和跨越频率强烈依赖于所研究的特定生物体。关于第二个问题，我们认为环丁烷二聚体可能是缓慢复制基因组中大多数突变的原因，这是由于胞嘧啶的脱氨作用，并且T-T以及在较小程度上T-C（6-4）加合物在快速复制病毒（如M13和λ噬菌体）的紫外线诱变中起更大作用。
