GltS regulates biofilm formation in methicillin-resistant Staphylococcus aureus

Impaired intake of exogenous glutamate, due to deficiency of the GltS sodium-glutamate transporter, promotes increased Staphylococcus aureus biofilm formation in vitro and in vivo. Biofilm-based infection is a major healthcare burden. Methicillin-resistant Staphylococcus aureus (MRSA) is one of major organisms responsible for biofilm infection. Although biofilm is induced by a number of environmental signals, the molecule responsible for environmental sensing is not well delineated. Here we examined the role of ion transporters in biofilm formation and found that the sodium-glutamate transporter gltS played an important role in biofilm formation in MRSA. This was shown by gltS transposon mutant as well as its complementation. The lack of exogenous glutamate also enhanced biofilm formation in JE2 strain. The deficiency of exogenous glutamate intake accelerated endogenous glutamate/glutamine production, which led to the activation of the urea cycle. We also showed that urea cycle activation was critical for biofilm formation. In conclusion, we showed that gltS was a critical regulator of biofilm formation by controlling the intake of exogenous glutamate. An intervention to target glutamate intake may be a potential useful approach against biofilm.

Automated summary

The deficiency of the sodium-glutamate transporter GltS impairs the intake of exogenous glutamate, leading to increased Staphylococcus aureus biofilm formation. Additionally, the lack of exogenous glutamate enhances endogenous glutamate/glutamine production and activates the urea cycle, which is critical for biofilm formation.