Abstract
Yersinia pseudotuberculosis forms biofilms on Caenorhabditis elegans which block nematode feeding. This genetically amenable host-pathogen model has important implications for biofilm development on living, motile surfaces. Here we show that Y. pseudotuberculosis biofilm development on C. elegans is governed by N-acylhomoserine lactone (AHL)-mediated quorum sensing (QS) since (i) AHLs are produced in nematode associated biofilms and (ii) Y. pseudotuberculosis strains expressing an AHL-degrading enzyme or in which the AHL synthase (ypsI and ytbI) or response regulator (ypsR and ytbR) genes have been mutated, are attenuated. Although biofilm formation is also attenuated in Y. pseudotuberculosis strains carrying mutations in the QS-controlled motility regulator genes, flhDC and fliA, and the flagellin export gene, flhA, flagella are not required since fliC mutants form normal biofilms. However, in contrast to the parent and fliC mutant, Yop virulon proteins are up-regulated in flhDC, fliA and flhA mutants in a temperature and calcium independent manner. Similar observations were found for the Y. pseudotuberculosis QS mutants, indicating that the Yop virulon is repressed by QS via the master motility regulator, flhDC. By curing the pYV virulence plasmid from the ypsI/ytbI mutant, by growing YpIII under conditions permissive for type III needle formation but not Yop secretion and by mutating the type III secretion apparatus gene, yscJ, we show that biofilm formation can be restored in flhDC and ypsI/ytbI mutants. These data demonstrate that type III secretion blocks biofilm formation and is reciprocally regulated with motility via QS.
Highlights
The human pathogenic Yersiniae (Yersinia pseudotuberculosis, Yersinia enterocolitica and Yersinia pestis) share a high degree of DNA identity, but cause distinct diseases ranging from enterocolitis (Y. enterocolitica and Y. pseudotuberculosis) to pneumonic, bubonic or septicaemic plague (Y. pestis)
We have discovered that quorum sensing is required for Y. pseudotuberculosis biofilm formation on C. elegans through a regulatory pathway which involves the master motility regulator protein (FlhDC) reciprocally controlling bacterial swimming and the construction of a specialized secretion needle that delivers proteins into mammalian cells to disrupt their normal activities
Y. pseudotuberculosis produces acylhomoserine lactone (AHL) when growing as a biofilm on the surface of C. elegans
Summary
The human pathogenic Yersiniae (Yersinia pseudotuberculosis, Yersinia enterocolitica and Yersinia pestis) share a high degree of DNA identity, but cause distinct diseases ranging from enterocolitis (Y. enterocolitica and Y. pseudotuberculosis) to pneumonic, bubonic or septicaemic plague (Y. pestis). Essential for the virulence of all pathogenic Yersiniae, is the ,70-kb pYV virulence plasmid, which encodes the Yop virulon. This consists of a type III secretion system which enables Yersinia to inject multiple Yop effector proteins directly into the cytosol of eukaryotic cells and so subvert host cell signalling pathways Biofilm formation is straindependent and a study of over 40 different Y. pseudotuberculosis strains showed that some formed biofilms on C. elegans but not on abiotic polystyrene surfaces and vice versa [6]. No relationship was observed between strains forming biofilms on C. elegans and those that formed biofilms on polystyrene surfaces. These findings suggest that biofilm development on the living surface of C. elegans is different from that on an abiotic surface such as polystyrene
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