Abstract
Mutation frequency decline (MFD) in Escherichia coli was examined for effects associated with genetic defects in mismatch repair. The kinetics of MFD are slower when the B/r strain WU3610 carries the mutation mutS201::Tn5 or mutL::Tn10, both of which affect mismatch repair. Similar slow kinetics are produced by mutH34 but not by mutH471::Tn5; the latter has no apparent effect. Strain WU3610-45 (mfd-1) produces the slower kinetics if transcription is inhibited during the post-UV incubation, although it produces no decline in normal circumstances. The slower kinetics are therefore attributed to bulk excision repair that remains when rapid transcription-coupled repair (TCR) is eliminated by certain defects in mismatch repair. A model is proposed wherein mismatch repair defects are thought to slow the activity of TCR but, unlike an mfd defect, not to impede dissociation of stalled transcription complexes at lesions in the transcribed DNA strand.
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