期刊名称：Proceedings of the National Academy of Sciences
印刷版ISSN：0027-8424
电子版ISSN：1091-6490
出版年度：1982
卷号：79
期号：13
页码：4123-4127
DOI：10.1073/pnas.79.13.4123
语种：English
出版社：The National Academy of Sciences of the United States of America
摘要：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.
