Abstract

UV‐radiation‐induced lesions in DNA result in the formation of: (1) excision gaps (i.e. a lesion is excised, leaving a gap), (2) daughter‐strand gaps (i.e. a lesion can be skipped during replication, leaving a gap), and (3) double‐strand breaks (i.e. the DNA strand opposite a gap can be cut). In Escherichia coli, the recA gene product is involved in repairs of all three types of lesions – repair of daughter‐strand gaps (2) and double‐strand breaks (3) constitutes post‐replication repair. The evidence suggests, furthermore, that recA‐dependent repair of excision gaps (1) produced in DNA replicated prior to UV irradiation (pre‐replication repair) appears to occur by similar mechanisms.