Accessory replicative helicases aid the primary replicative helicase in duplicating
protein-bound
DNA, especially transcribed
DNA. Recombination
enzymes also aid genome duplication by facilitating the repair of DNA lesions via strand exchange and also processing of blocked fork
DNA to generate structures onto which the replisome can be reloaded. There is significant interplay between accessory helicases and recombination
enzymes in both bacteria and lower eukaryotes but how these replication repair systems interact to ensure efficient genome duplication remains unclear. Here, we demonstrate that the
DNA content defects of Escherichia coli cells lacking the strand exchange
protein RecA are driven primarily by conflicts between replication and transcription, as is the case in cells lacking the accessory helicase Rep. However, in contrast to Rep, neither RecA nor RecBCD, the helicase/
exonuclease that loads RecA onto dsDNA ends, is important for maintaining rapid
chromosome duplication. Furthermore, RecA and RecBCD together can sustain viability in the absence of accessory replicative helicases but only when transcriptional barriers to replication are suppressed by an
RNA polymerase mutation. Our data indicate that the minimisation of replisome pausing by accessory helicases has a more significant impact on successful completion of
chromosome duplication than recombination-directed fork repair.