Gamma irradiation triggers a global stress response in Escherichia coli O157:H7 including base and nucleotides excision repair pathways

Shiga toxin-producing Escherichia coli O157:H7, one of the most severe human foodborne pathogens, can withstand several stresses, including some levels of γ-irradiation. In this study, the response of E. coli O157:H7 to a sensitization irradiation dose of 0.4 kGy was assessed using RNA-seq transcriptomic at 10 (t10) and 60 (t60) min post-irradiation, combined with an isobaric tags for relative and absolute quantitation (iTRAQ) proteomic analysis at 60 min post-irradiation. Several functions were induced by the treatment, such as base excision repair and nucleotide excision repair pathways; sulfur and histidine metabolism, and virulence mechanisms. Additionally, the sulA gene, coding for the cell division repressor, together with other genes involved in SOS response and repair mechanism (including recA, recN, recJ, recQ, mutM and uvrB) were up-regulated at t60. As the early response to irradiation stress (t10), dnaK, groEL, ibpA, sulfur metabolism genes, as well as those related to oxidative stress were up-regulated, while histidine biosynthesis genes were down-regulated. Acid stress, heat shock, UV resistance and several virulence genes, especially stx2A/stx2b which code for the Shiga toxins characteristic of O157:H7, were upregulated at 60 min post-irradiation. The treatment was also found to increase the levels of CysN, MutM, DinG and DnaC in the cells, proteins involved respectively in sulfur metabolism, base excision repair, recombinational DNA repair and chromosome replication. Our results provide insights into the resistance response of E. coli O157:H7 to a non-lethal irradiation dose. Our findings indicate that E. coli O157:H7 can resist to γ-irradiation through important modifications in genes expression and proteins profiles.