The ArcR contributes to the biofilm formation of Staphylococcus aureus by promoting PIA synthesis

Staphylococcus aureus ArcR is a conserved member of Crp/Fnr regulatory family, which has previously been reported to activate the transcription of the arginine deiminase (ADI) pathway operon arcABDC. However, little is known about its impact on biofilm formation. Here, we show that ArcR contributes to polysaccharide intercellular adhesin (PIA) biosynthesis and biofilm formation in S. aureus. Crystal violet biofilms staining, confocal laser scanning microscopy (CLSM), and flow-based biofilm assays collectively demonstrated that deletion of arcR in S. aureus significantly attenuated biofilm formation under both static and flow conditions. The inactivation of arcR reduced the amount of polysaccharide intercellular adhesin (PIA), which is a momentous component in the Staphylococcal biofilm. Consistently, in the arcR deletion mutant strain, the expression levels of icaA and icaD in ica operon responsible for PIA synthesis were significantly down-regulated, and icaR, which is the repress regulator of the ica operon, was significantly up-regulated. The suppression of ArcR on icaR transcription was further verified by LacZ reporter assay. Additionally, analyses found that autolysis mediated eDNA release was increased via an as yet undefined pathway, while this process is independently of AtlA expression. Collectively, our results demonstrate the positive influence of ArcR on biofilm formation by promoting PIA synthesis, suggesting that arcR may serve as a potential target for the treatment of biofilm-associated infections.