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Abstract
Quorum sensing (QS) is a cell-to-cell communication process that regulates major pathogenic
attributes in bacteria including biofilm formation, secretion of virulence factors,
and antimicrobial resistance. The two-component Fsr-QS system of the nosocomial pathogen
Enterococcus faecalis controls the production of extracellular gelatinase that contributes
to biofilm development by enhancing the release of nucleic acids into the biofilm
matrix. However, the contribution of this system to the deposition of other biofilm
matrix components such as polysaccharides and proteins remains unknown. Using wild
type and mutant strains, we discovered that biofilm formation was attenuated by inactivation
of the Fsr system or its downstream gelatinase production. Inactivation of the Fsr
system caused a modest, yet significant reduction in biofilm metabolic activity without
affecting cell counts. Inactivation of the QS-signal sensor FsrC and response regulator
FsrA resulted in decreased extracellular polysaccharides and proteins in biofilms
in a temporal manner. Irrespective of biofilm age, eDNA levels were reduced in the
gelatinase mutant strain. Our results collectively suggest that the Fsr system contributes
to the temporal deposition of polysaccharides and proteins into the extracellular
polymeric matrix (EPS) of E. faecalis biofilm, without affecting bacterial viability.
This understanding of the role of the Fsr-QS system in biofilm development may reveal
a novel target to develop effective antibiofilm agents to tackle E. faecalis-mediated
infections such as in dental root canals, heart valves, and surgical sites.