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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.

Biofilm Development on Caenorhabditis elegans by Yersinia Is Facilitated by Quorum Sensing-Dependent Repression of Type III Secretion