(group B ; GBS) is a common inhabitant of the genitourinary and/or gastrointestinal tract in up to 40% of healthy adults; however, this opportunistic pathogen is able to breach restrictive host barriers to cause disease and persist in harsh and changing conditions. This study sought to identify a role for quorum sensing, a form of cell to cell communication, in the regulation of the fibrinogen-binding () two-component system and the ability to associate with decidualized endometrial cells in vitro. To do this, we created a deletion in , which encodes the putative autoinducing peptide, in a GBS strain belonging to multilocus sequence type (ST)-17 and made comparisons to the wild type. Sequence variation in the operon was detected in 40 clinical strains and a non-synonymous single nucleotide polymorphism was detected in in all of the ST-17 genomes that resulted in a truncation. Using qPCR, expression of operon genes was significantly decreased in the ST-17 mutant during exponential growth with the biggest difference (3.3-fold) occurring at higher cell densities. Association with decidualized endometrial cells was decreased 1.3-fold in the mutant relative to the wild type and expression was reduced 22-fold in following exposure to the endometrial cells. Collectively, these data suggest that this putative quorum sensing molecule is important for attachment to human tissues and demonstrate a role for RgfD in GBS pathogenesis through regulation of .

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5295018PMC
http://dx.doi.org/10.3390/genes8010023DOI Listing

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