ArcR contributes to tolerance to fluoroquinolone antibiotics by regulating katA in Staphylococcus aureus .

is an opportunistic pathogen that shows a unique ability to quickly respond to a variety of antibiotics. The Crp/Fnr family transcriptional regulator ArcR controls expression of arginine deiminase pathway genes , which enable the utilization of arginine as an energy source for cell growth under anaerobic conditions. However, ArcR shares low overall similarity with other Crp/Fnr family proteins, suggesting that they differ in the response to environmental stress. In this study, MIC and survival assays were performed to determine the role of ArcR in antibiotic resistance and tolerance. The results showed that deletion of reduced tolerance of to fluoroquinolone antibiotics, mainly through a defect in the response to oxidative stress. In mutant, the expression of the major catalase gene was downregulated, and overexpression restored bacterial resistance to oxidative stress and antibiotics. We showed that ArcR directly regulated transcription by binding to the promoter region of . Therefore, our results revealed the contribution of ArcR in bacterial tolerance to oxidative stress and subsequently to fluoroquinolones antibiotics. This study added our understanding on the role of Crp/Fnr family in bacterial susceptibility to antibiotics.