The SMC like protein RecN is at the crossroads of Genotoxic Stress Responses in Escherchia coli
DNA damage repair (DDR) is an essential process for living organisms, it contributes to genome maintenance and evolution. DDR involves different pathways including Homologous recombination (HR), Nucleotide Excision Repair (NER) and Base excision repair (BER) for example.  The activity of each pathway is revealed in particular contexts but they also intervene concomitantly or subsequently to repair most DNA lesions. In the present study, we used two genotoxic antibiotics, mitomycin C (MMC) and Bleomycin (BLM), to decipher the interplays between these different pathways in E. coli. We demonstrated that only a small set of DDR proteins are common to the repair of the lesions induced by these two drugs. Among them, RecN, an SMC like protein, plays an important role by controlling sister chromatids dynamics and genome morphology at different steps of the repair processes. We demonstrated that RecN's influence on sister chromatids dynamics is not equivalent during the processing of the lesions induced by the two drugs. We observed that RecN activity and stability requires a pre-processing of the MMC-induced lesions by the NER but not for BLM-induced lesions. In addition to its well-known importance to engage cells in the HR pathway to save cells presenting double strand breaks, our results show that RecN plays a major role in rescuing toxic intermediates generated by the BER pathway. Overall design: Transposon Insertion Sequencing (TIS)