Tessman I, Liu S K, Kennedy M A
Department of Biological Sciences, Purdue University, West Lafayette, IN 47907.
Proc Natl Acad Sci U S A. 1992 Feb 15;89(4):1159-63. doi: 10.1073/pnas.89.4.1159.
We measured the kinetics of growth and mutagenesis of UV-irradiated DNA of phages S13 and lambda that were undergoing SOS repair; the kinetics strongly suggest that most of SOS mutagenesis arises from the deamination of cytosine in cyclobutane pyrimidine dimers, producing C----T transitions. This occurs because the SOS mechanism bypasses T--T dimers promptly, while bypass of cytosine-containing dimers is delayed long enough for deamination to occur. The mutations are thus primarily the product of a faithful mechanism of lesion bypass by a DNA polymerase and are not, as had been generally thought, the product of an error-prone mechanism. All of these observations are explained by the A-rule, which is that adenine nucleotides are inserted noninstructionally opposite DNA lesions.
我们测量了正在进行SOS修复的噬菌体S13和λ的紫外线照射DNA的生长和诱变动力学；动力学有力地表明，大多数SOS诱变源于环丁烷嘧啶二聚体中胞嘧啶的脱氨作用，产生C→T转换。发生这种情况是因为SOS机制能迅速绕过T-T二聚体，而含胞嘧啶二聚体的绕过则延迟足够长的时间以使脱氨作用发生。因此，这些突变主要是DNA聚合酶忠实的损伤绕过机制的产物，而并非如普遍认为的那样，是易错机制的产物。所有这些观察结果都可以用A规则来解释，即腺嘌呤核苷酸在DNA损伤的对面无指令地插入。
