RecN protein and transcription factor DksA combine to promote faithful recombinational repair of DNA double-strand breaks.
In rapidly dividing bacterial cells, the machinery for repair of DNA double-strand breaks has to contend not only with the forces driving replication and transmission of the DNA but also its transcription. By exploiting I-SceI homing endonuclease to break the Escherichia coli chromosome at one or more defined locations, we have been able to investigate how these processes are co-ordinated and repair is accomplished. When breaks are induced at a single site, the SOS-inducible RecN protein and the transcription factor DksA combine to promote efficient repair. When induced at two or more, distantly located sites, RecN becomes almost indispensable. Many cells that do survive have extensive deletions of sequences flanking the break, with end points often coinciding with imperfect repeat elements. These findings herald a much greater complexity for chromosome repair than suggested by current mechanistic models and reveal a role for RecN in protecting the chromosome from break-induced chromosome rearrangements.