Modulation of DNA damage tolerance in E scherichia coli recG and ruv strains by mutations affecting PriB , the ribosome and RNA polymerase

• Published in: Molecular microbiology 2012-11, Vol.86 (3), p.675-691
• Main Authors: Mahdi, Akeel A., Briggs, Geoffrey S., Lloyd, Robert G.
• Format: Article
• Language: English
• ISSN: 0950-382X; 1365-2958
• DOI: 10.1111/mmi.12010

RecG is a DNA translocase that helps to maintain genomic integrity. Initial studies suggested a role in promoting recombination, a possibility consistent with synergism between recG and ruv null alleles and reinforced when the protein was shown to unwind H olliday junctions. In this article we describe novel suppressors of recG and show that the pathology seen without RecG is suppressed on reducing or eliminating PriB , a component of the PriA system for replisome assembly and replication restart. Suppression is conditional, depending on additional mutations that modify ribosomal subunit S 6 or one of three subunits of RNA polymerase. The latter suppress phenotypes associated with deletion of priB , enabling the deletion to suppress recG . They include alleles likely to disrupt interactions with transcription anti‐terminator, NusA . Deleting priB has a different effect in ruv strains. It provokes abortive recombination and compromises DNA repair in a manner consistent with PriB being required to limit exposure of recombinogenic ssDNA . This synergism is reduced by the RNA polymerase mutations identified. Taken together, the results reveal that RecG curbs a potentially negative effect of proteins that direct replication fork assembly at sites removed from the normal origin, a facility needed to resolve conflicts between replication and transcription.