Mutation frequency decline (MFD) in Escherichia 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 < > 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 < > 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.