Mutation frequency decline in Escherichia coli .2. Kinetics support the involvement of transcription coupled excision repair

Mutation frequency decline (MFD) in Eschel ichia coli was examined to demonstrate repair of targeting photoproducts during the post-UV incubation required in this process. Repair of mutation-targeting cyclobutane pyrimidine dimers (T lozenge C) was demonstrated when a correlation was established between the mutation frequency normally associated with these lesions and the rate of mutation production at these lesions by spontaneous deamination of cytosines and photoreversal in ung-defective cells. An incubation producing a decline in mutation frequency, i.e., MFD, also produces lower rates of mutation increase via the deamination mechanism. Since the latter assay involves processes entirely within the post-UV incubation period, the lower rates are attributed to rapid transcription-coupled nucleotide excision repair (TCR) that reduces the number of relevant T lozenge C dimers during this period. Rediscovery of the neglected fact that MFD can be stimulated by post-UV incubation in buffer alone is part of the analysis. Results presented here and a variety of others are discussed to support a model of MFD as a particular example of TCR: effective repair of photoproducts in the transcribed DNA strand that target glutamine tRNA suppressor mutations occurs during the appropriate post-UV incubation and is responsible for MFD.