Abstract
The lacI forward mutagenesis system was used to determine the mutational specificity of UV-induced mutation in a repair-proficient (Uvr+) and a repair-deficient (.DELTA.UvrB) strain of E. 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.cntdot.C .fwdarw. A.cntdot.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. DNA structure apparently plays an important role in determining the fate of UV-induced premutational lesions.