The Quorum Sensing System of Yersinia enterocolitica 8081 Regulates Swimming Motility, Host Cell Attachment, and Virulence Plasmid Maintenance

Abstract

Although <i>Yersinia enterocolitica</i> genomes are highly heterogeneous, they contain a conserved <i>N</i>-acylhomoserine lactone-dependent (AHL) quorum sensing (QS) system consisting of the <i>luxR</i> and <i>luxI</i> orthologs <i>yenR</i> and <i>yenI</i> respectively. Certain hypervirulent strains also contain a putative orphan <i>luxR</i> gene, <i>ycoR</i>, that is not linked to an AHL synthase. To explore the contribution of <i>yenR/yenI/ycoR</i> to QS-dependent phenotypes in <i>Yersinia enterocolitica</i> strain 8081, single and multiple mutants were constructed. AHL profiling identified <i>N</i>-(3-oxohexanoyl) homoserine lactone, <i>N</i>-hexanoylhomoserine lactone, and <i>N</i>-(3-oxoseptanoyl) homoserine lactone as the most abundant. The AHL profiles of the <i>yenR</i>, <i>ycoR</i> and <i>yenR/ycoR</i> mutants were similar to the parent suggesting that the two LuxR homologues do not regulate AHL production while the <i>yenI</i> mutants were AHL-negative. A role for QS in swimming motility and cell attachment was demonstrated. Down-regulation of the virulence plasmid partition gene, <i>spyA</i>, in <i>yenI</i> and <i>yenI</i>/<i>yenR</i>/<i>ycoR</i> mutants is consistent with the greater loss of the <i>Y. enterocolitica</i> pYVe virulence plasmid in the <i>yenI</i> mutant during serial passage at 37 &deg;C but not at 22 &deg;C. A role for QS-regulated <i>spyA</i> in virulence plasmid maintenance is suggested.