In this study, however, we showed that xthA nfo mutant bacteria were sensitive to BLM. This discrepancy is most probably because the single xthA and nfo mutant cells are not as sensitive as the double mutant. The sensitivity of recG and recN mutant strains growing in broth to BLM was confirmed. These mutant strains are not sensitive to other commonly used DNA damaging agents such as ultra-violet light or the methylating agents, ethyl- and methyl methane sulfonate. BLM must cause a specific DNA lesion that requires RecG and RecN and which is not produced by other commonly used DNA damaging agents. In the absence of RecBCD, recN mutant strains are sensitive to ionizing radiation, but not ultra-violet light, suggesting a role in repair of DSBs and/ or oxidative damage through the RecF pathway. Transcription of the recN gene is strongly stimulated during the SOS response. However, the function of the recN gene product remains unknown although it is a member of the SMC family of proteins. RecG is a Lomitapide Mesylate helicase that can translocate Holliday junctions but in the opposite direction to RuvAB. recG mutants are only slightly sensitive to ultra-violet light or X-rays but show increased sensitivity in a ruvAB mutant background. Recently, Rudolph et al. proposed that RecG prevents PriA mediated overreplication of UV-irradiated chromosomal DNA. In the absence of RecG, extensive replication GSK 650394 occurs at chromosomal sites where replication forks have been inactivated. New forks are initiated through the action of PriA, which can load the DnaC protein, which in turn can load the replicative DnaB helicase. It is possible that such a ����pathological cascade��’may also occur in recG cells exposed to BLM. Alternatively, RecG might unwind persistent recombination intermediates that would otherwise compromise chromosome replication. In contrast to bacteria growing in broth, cells growing in glucose minimal medium were resistant to the cytotoxic effects of BLM. This result was not expected as other DNA-damaging agents are effective in both types of media. Single-strand breaks were formed in E. coli cells growing in minimal medium based on the increased sensitivity to BLM of ligase-deficient strains. Alternatively, the requirement for DNA ligase in both broth and minimal medium might reflect the increased need for this enzyme as a result of base excision repair of lesions. There is no requirement for homologous recombination functions and only a weak SOS response in wildtype cells exposed to BLM. The sensitivity of the ligase-deficient strains would minimize, but not exclude, the possibility of reduced transport of BLM into the cell as an explanation for resistance. The lack of BLM sensitivity for cells growing in minimal medium could be due to the reduced number of replication forks in such cells as compared to those grown in broth. Fewer forks would reduce encounters with lesions to form DSBs.