A model for the recA-dependent repair of excision gaps in UV-irradiated Escherichia coli.

We have tested and supported the hypothesis that, in UV-irradiated Escherichia coli, recA-dependent nucleotide excision repair only functions in the replicated portion of the chromosome (i.e., where sister duplexes exist). Using a dnaA(Ts) mutation to align the chromosomes (i.e., all rounds of DNA replication were completed, and new rounds could not be initiated), we studied the genetic control of excision repair (measured as the repair of excision gaps in DNA) in cells with unreplicated chromosomes, and also in cells with partially replicated chromosomes. The excision repair that occurred in cells with unreplicated chromosomes was recA independent, but the excision repair that occurred in cells with partially replicated chromosomes was partially recA dependent. We found no evidence of interchromosomal recombination in recA-dependent excision repair. The majority of this recA-dependent excision repair was recF dependent, and a small portion was recB dependent. The recF and recB genes are suggested to function in excision repair in a manner similar to their function in postreplication repair, i.e., in the replicated portion of a chromosome, the RecF pathway repairs gaps, and the RecB pathway repairs the DNA double-strand breaks that arise at unrepaired gaps.