Todd P A, Glickman B W
Proc Natl Acad Sci U S A. 1982 Jul;79(13):4123-7. doi: 10.1073/pnas.79.13.4123.
We used the lacI forward mutagenesis system to determine the mutational specificity of UV-induced mutation in a repair-proficient (Uvr+) and a repair-deficient (delta UvrB) strain of Escherichia coli. The spectra recovered at similar levels of mutagenesis were similar, the exception being a mutational hotspot at site A24 specific to the delta UvrB strain. Mutations induced at this hotspot, as well as those induced at other mutational hotspots that were found to be common to both the Uvr+ and Uvr- strains, involve G . C leads to A . T transitions. All of the hotspots are at sites of potential dipyrimidine photoproducts, such as thymine-cytosine and cytosine-cytosine dimers, or of pyrimidine-cytosine photoproduct Py-C lesions. Each of these hotspots occurs at a site in the potential hairpin loop of quasi-palindromic sequences. These observations suggest an important role for DNA structure in determining the fate of UV-induced premutational lesions.
我们使用乳糖抑制子正向诱变系统来确定紫外线诱导的突变在大肠杆菌的修复 proficient(Uvr+)和修复缺陷(ΔUvrB)菌株中的突变特异性。在相似诱变水平下恢复的光谱相似,唯一的例外是ΔUvrB菌株特有的A24位点的一个突变热点。在这个热点诱导的突变,以及在Uvr+和Uvr-菌株中都发现的其他突变热点诱导的突变,都涉及G.C到A.T的转换。所有热点都位于潜在的二嘧啶光产物位点,如胸腺嘧啶 - 胞嘧啶和胞嘧啶 - 胞嘧啶二聚体,或嘧啶 - 胞嘧啶光产物Py - C损伤位点。这些热点中的每一个都出现在准回文序列潜在发夹环的一个位点上。这些观察结果表明DNA结构在决定紫外线诱导的前突变损伤的命运中起重要作用。