Description:
<jats:title>ABSTRACT</jats:title><jats:p>The β-glucoside cellobiose has been reported to specifically repress the PrfA-dependent virulence genes<jats:italic>hly</jats:italic>and<jats:italic>plcA</jats:italic>in<jats:italic>Listeria monocytogenes</jats:italic>NCTC 7973. This led to the hypothesis that β-glucosides, sugars of plant origin, may act as signal molecules, preventing the expression of virulence genes if<jats:italic>L. monocytogenes</jats:italic>is living in its natural habitat (soil). In three other laboratory strains (EGD, L028, and 10403S), however, the effect of cellobiose was not unique, and all fermentable carbohydrates repressed<jats:italic>hly</jats:italic>. This suggested that the downregulation of virulence genes by β-glucosides is not a specific phenomenon but, rather, an aspect of a global regulatory mechanism of catabolite repression (CR). We assessed the effect of carbohydrates on virulence gene expression in a panel of wild-type isolates of<jats:italic>L. monocytogenes</jats:italic>by using the PrfA-dependent phospholipase C gene<jats:italic>plcB</jats:italic>as a reporter. Utilization of any fermentable sugar caused<jats:italic>plcB</jats:italic>repression in wild-type<jats:italic>L. monocytogenes</jats:italic>. However, an EGD variant was identified in which, as in NCTC 7973,<jats:italic>plcB</jats:italic>was only repressed by β-glucosides. Thus, the regulation of<jats:italic>L. monocytogenes</jats:italic>virulence genes by sugars appears to be mediated by two separate mechanisms, one presumably involving a CR pathway and another specifically responding to β-glucosides. We have identified in<jats:italic>L. monocytogenes</jats:italic>a 4-kb operon,<jats:italic>bvrABC</jats:italic>, encoding an antiterminator of the BglG family (<jats:italic>bvrA</jats:italic>), a β-glucoside-specific enzyme II permease component of the phosphoenolpyruvate-sugar phosphotransferase system (<jats:italic>bvrB</jats:italic>), and a putative ADP-ribosylglycohydrolase (<jats:italic>bvrC</jats:italic>). Low-stringency Southern blots showed that this locus is absent from other<jats:italic>Listeria</jats:italic>spp. Transcription of<jats:italic>bvrB</jats:italic>was induced by cellobiose and salicin but not by arbutin. Disruption of the<jats:italic>bvr</jats:italic>operon by replacing part of<jats:italic>bvrAB</jats:italic>with an interposon abolished the repression by cellobiose and salicin but not that by arbutin. Our data indicate that the<jats:italic>bvr</jats:italic>locus encodes a β-glucoside-specific sensor that mediates virulence gene repression upon detection of cellobiose and salicin. Bvr is the first sensory system found in<jats:italic>L. monocytogenes</jats:italic>that is involved in environmental regulation of virulence genes.</jats:p>