The cyclic adenosine monophosphate-ArcRsa signaling axis modulates biofilm formation in dairy-derived Staphylococcus aureus via transcriptional repression of ica operon.
TL;DR
Functional crosstalk between cAMP and ArcRsa through direct regulation at the gene icaA promoter is demonstrated, supporting an essential regulatory role for the cAMP-ArcRsa signaling module in modulating biofilm formation in S. aureus.
Abstract
Staphylococcus aureus has significantly contributed to the contamination of dairy products and preserved foods, attributed to its ability to colonize a wide range of environments and form biofilms. ArcR, the Crp/Fnr family regulatory protein in S. aureus plays key roles in various biological processes. However, the molecular mechanism underlying biofilm regulation by the cAMP-ArcRsa complex remains poorly defined. In this work, we investigated the biological function of ArcRsa in mediating biofilm formation in dairy-derived S. aureus RMSA49. The results demonstrated that the deletion of arcRsa resulted in a dramatic increase in biofilm formation. An in-depth dissection of the regulatory mechanism of ArcRsa revealed that it negatively regulates the production of the polysaccharide intercellular adhesin (PIA) by directly binding to the promoter of the gene icaA. Further analysis revealed that cAMP-ArcRsa complex support biofilm maintenance of S. aureus RMSA 49 by strengthening its regulation of genes icaA. ArcRsa controls the transcription of its own gene and icaA by attaching to specific sequences at the site arcRsa (5'-ATCACGCGACAA-3') and site arcRsa2 (5'-ATTAAGTTGCAA-3'). Our results demonstrate functional crosstalk between cAMP and ArcRsa through direct regulation at the gene icaA promoter, supporting an essential regulatory role for the cAMP-ArcRsa signaling module in modulating biofilm formation in S. aureus.