Pfs promotes autolysis-dependent release of eDNA and biofilm formation in Staphylococcus aureus.

Staphylococcus aureus is a major biofilm-forming pathogen, and biofilm formation remains an obstacle in the treatment of clinical S. aureus infection. Methylthioadenosine/S-adenosylhomocysteine nucleosidase (Pfs) has been implicated in methylation reactions, polyamine synthesis, vitamin synthesis, and quorum-sensing pathways. In this study, we observed that the deletion of pfs gene in S. aureus NCTC8325 reduced bacterial clumping ability and resulted in the decreased biofilm formation under both static and dynamic flow conditions in an autoinducer-2-independent manner. While the PIA amount was not affected, the pfs mutation significantly decreased the amount of eDNA present in the biofilm and the cell autolysis. Consistent with reduced autolysis, the transcription levels of the autolysin genes, lytM and atlE, were reduced in the absence of Pfs. These data suggest that Pfs promotes autolysis-dependent release of eDNA and biofilm formation in S. aureus, and our findings indicate that Pfs is a potential novel target for anti-biofilm therapy.