## 1 Introduction
For example, the _xrep_\(\Delta\)_uvrD_ double mutant suppressor _rpoB*35_ allows cells unable to synthesise (p)ppGpp to grow on minimal medium, a so-called stringent phenotype which indicates that _rpoB*35_ phenocopies elevated (p)ppGpp [22; 79]. _rpoB*35_ may also destabilise transcription complexes stalled by nucleotide starvation or DNA lesions [42] although this has been questioned and data presented indicating this mutant RNA polymerase has a reduced probability of backtracking [80]. Another class of mutations provide weaker suppression of _xrep_\(\Delta\)_uvrD_ double mutant inviability. These suppressors have defects in the RecA loading factors RecF, RecO or RecR or in RecJ exonuclease or RecQ helicase, all of which facilitate RecA loading onto single-stranded DNA gaps [22; 30; 81; 82]. This suppression may reflect the potential for toxic levels of RecFORQJ-dependent strand exchange by RecA at blocked forks [81; 83; 84]. In _xrep_\(\Delta\)_uvrD_ double mutant cells, elevated fork pausing together with the lack of UvrD-catalysed disruption of RecA-ssDNA filaments may explain why ablation of RecFORQJ-dependent RecA loading partially suppresses _xrep_\(\Delta\)_uvrD_ double mutant inviability. However, UvrD cannot counter the adverse effects of RecAFORQJ in _xrep_ mutant cells [64] implying that lack of RecA-ssDNA turnover is not the primary reason why RecAFORQJ is so toxic in _xrep_\(\Delta\)_uvrD_ mutant cells. The relative importance of accessory helicases and recombination enzymes for genome duplication remains unclear. _E. coli_ cells lacking RecA or RecBCD have reduced viability [85]. Cells bearing inverted _rrn_ operons do not require Rep for viability but do require either RecBCD helicase/exonuclease or RecBCD helicase lacking exonuclease activity plus RecA [30; 73]. These data suggest that RecBCD and RecA have a more important role in replicating the chromosome than Rep. However, during normal growth without inverted highly expressed operons there is insufficient recombination to require Holliday junction resolution for viability [86]. Only in the absence of Rep does this resolution become important for viability [64], consistent with Rep having a primary role in sustaining completion of chromosome replication. Here we show that the known chromosome content defects of _recA_ cells is driven primarily by transcription, mirroring the importance of transcriptional barriers to replication in the chromosome content defects of _xrep_ mutant cells [6]. Both RecA and Rep therefore have roles in mitigating the impact of transcription on genome duplication. However, in contrast to Rep [31], neither RecA nor RecBCD play important roles in sustaining wild type chromosome duplication times. These data indicate that accessory helicases play a more significant role than recombination enzymes in sustaining rapid chromosome duplication. This view is supported by RecA and RecBCD being able to sustain viability in the absence of Rep and UvrD but only in the presence of an RNA polymerase mutation that alleviates transcriptional barriers to replication. Furthermore, both RecA and RecBCD are needed for this viability, indicating that RecBCD-catalysed DNA degradation in the absence of RecA loading does not provide an efficient means of sustaining chromosome duplication. We conclude that accessory helicases are more important than recombination enzymes for replicating the _E. coli_ chromosome but that replicative barriers normally dealt with by accessory helicases can be surmounted by less efficient mechanisms via recombination enzymes.