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Two-component systems (TCS) are modular signal transduction pathways that allow cells to adapt to prevailing environmental conditions by modifying cellular physiology.  Staphylococcus aureus  has 16 TCSs to adapt to the diverse microenvironments encountered during its life cycle, including host tissues and implanted medical devices.  S. aureus  is particularly prone to cause infections associated to medical devices, whose surfaces coated by serum proteins constitute a particular environment. Identification of the TCSs involved in the adaptation of  S. aureus  to colonize and survive on the surface of implanted devices remains largely unexplored. Here, using an  in vivo  catheter infection model and a collection of mutants in each non-essential TCS of  S. aureus , we investigated the requirement of each TCS for colonizing the implanted catheter. Among the 15 mutants in non-essential TCSs, the  arl  mutant exhibited the strongest deficiency in the capacity to colonize implanted catheters. Moreover, the  arl  mutant was the only one presenting a major deficit in PNAG production, the main exopolysaccharide of the  S. aureus  biofilm matrix whose synthesis is mediated by the  icaADBC  locus. Regulation of PNAG synthesis by ArlRS occurred through repression of IcaR, a transcriptional repressor of  icaADBC  operon expression. Deficiency in catheter colonization was restored when the  arl  mutant was complemented with the  icaADBC  operon. MgrA, a global transcriptional regulator downstream ArlRS that accounts for a large part of the  arlRS  regulon, was unable to restore PNAG expression and catheter colonization deficiency of the  arlRS  mutant. These findings indicate that ArlRS is the key TCS to biofilm formation on the surface of implanted catheters and that activation of PNAG exopolysaccharide production is, among the many traits controlled by the ArlRS system, a major contributor to catheter colonization.

A Systematic Evaluation of the Two-Component Systems Network Reveals That ArlRS Is a Key Regulator of Catheter Colonization by Staphylococcus aureus