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Background  The global regulatory system ArcAB controls the anaerobic growth of  E. coli , however, its role in aerobic conditions is not well characterized. We have previously reported that ArcA was necessary for  Salmonella  to resist reactive oxygen species (ROS) in aerobic conditions.    Results  To investigate the mechanism of ROS resistance mediated by ArcAB, we generated deletion mutants of ArcA and ArcB in  E. coli . Our results demonstrated that both ArcA and ArcB were necessary for resistance to hydrogen peroxide (H 2 O 2 ), a type of ROS, and their function in this resistance was independent from H 2 O 2  scavenge. Mutagenesis analysis of ArcA indicated that ROS resistance was mediated through a distinct signaling pathway from that used in anaerobic conditions. An abundant protein flagellin was elevated at both the protein and mRNA levels in the  ΔarcA  mutant as compared to the wild type  E. coli , and deletion of flagellin restored the resistance of the  ΔarcA  mutant to H 2 O 2 . The resistance of the  ΔarcA  mutant  E. coli  to H 2 O 2  can also be restored by amino acid supplementation, suggesting that a deficiency in amino acid and/or protein synthesis in the mutant contributed to its susceptibility to H 2 O 2 , which is consistent with the notion that protein synthesis is necessary for ROS resistance.    Conclusion  Our results suggest that in addition to its role as a global regulator for anaerobic growth of bacteria, ArcAB system is also important for bacterial resistance to ROS in aerobic conditions, possibly through its influence on bacterial metabolism, especially amino acid and/or protein assimilation and synthesis.

Role of the ArcAB two-component system in the resistance of Escherichia colito reactive oxygen stress