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It has been shown that, following permeation of cell barriers, Cr(VI) killsB. subtilis cells following a mechanism of reactive oxygen species-promoted DNA damage, which is counteracted by the guanine oxidized repair system. Here we report a distinct mechanism of Cr(VI)-promoted DNA damage that involves production of DPCs capable of eliciting the bacterial SOS response. We also report that the NER and homologous recombination (RecA) repair pathways, as well as low-fidelity DNA polymerases, counteract this metal-induced mechanism of killing inB. subtilis . Hence, our results contribute to an understanding of how environmental pollutants activate global programs of gene expression that allow bacteria to contend with the cytotoxic and genotoxic effects of heavy metals.

Roles of Bacillus subtilis RecA, Nucleotide Excision Repair, and Translesion Synthesis Polymerases in Counteracting Cr(VI)-Promoted DNA Damage