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Abstract
Although Yersinia enterocolitica genomes are highly heterogeneous, they contain a conserved N-acylhomoserine lactone-dependent (AHL) quorum sensing (QS) system consisting of the luxR and luxI orthologs yenR and yenI respectively. Certain hypervirulent strains also contain a putative orphan luxR gene, ycoR, that is not linked to an AHL synthase. To explore the contribution of yenR/yenI/ycoR to QS-dependent phenotypes in Yersinia enterocolitica strain 8081, single and multiple mutants were constructed. AHL profiling identified N-(3-oxohexanoyl) homoserine lactone, N-hexanoylhomoserine lactone, and N-(3-oxoseptanoyl) homoserine lactone as the most abundant. The AHL profiles of the yenR, ycoR and yenR/ycoR mutants were similar to the parent suggesting that the two LuxR homologues do not regulate AHL production while the yenI mutants were AHL-negative. A role for QS in swimming motility and cell attachment was demonstrated. Down-regulation of the virulence plasmid partition gene, spyA, in yenI and yenI/yenR/ycoR mutants is consistent with the greater loss of the Y. enterocolitica pYVe virulence plasmid in the yenI mutant during serial passage at 37 °C but not at 22 °C. A role for QS-regulated spyA in virulence plasmid maintenance is suggested.
Highlights
Bacterial populations respond to external stimuli by producing and transducing chemical signal molecules in a cell density-dependent process known as quorum sensing (QS)
This consists of a type III secretion system (T3SS) which facilitates the injection of multiple Yersinia outer protein (Yop) effector proteins directly into the cytosols of eukaryotic cells to subvert host cell signalling pathways
We show that the yenI/yenR/ycoR QS system in Y. enterocolitica strain 8081 contributes to motility, eukaryotic cell attachment, and maintenance of the type III secretion system (TTSS) virulence plasmid, pYVe
Summary
Bacterial populations respond to external stimuli by producing and transducing chemical signal molecules in a cell density-dependent process known as quorum sensing (QS). The three Yersinia species that are pathogenic for humans are psychrotrophic and grow well between 4 ◦ C and 42 ◦ C and, as such, are well adapted to survive outside their mammalian hosts Upon infection they adapt rapidly to a temperature shift to 37 ◦ C where they cause differing. The virulence of the pathogenic Yersinia depends on the presence of an ~70-kb virulence plasmid, termed pYve, in Y. enterocolitica that encodes the Yersinia outer protein (Yop) virulon. This consists of a type III secretion system (T3SS) which facilitates the injection of multiple Yop effector proteins directly into the cytosols of eukaryotic cells to subvert host cell signalling pathways. T3SS is tightly regulated by environmental conditions and, in particular, the Ca2+ ion concentration and temperature which ensures that Yops are normally secreted at 37 ◦ C but not at 22 ◦ C (for reviews see [3,4,5])
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