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

PLoS Pathogens

George W. P. Joshua¹  Brendan W. Wren¹  Steve Atkinson²  Hannah L. Patrick²  Chien-Yi Chang²  Miguel Cámara²  Robert J. Goldstone²  Paul Williams² 

[1] Department of Infectious and Tropical Diseases, London School of Hygiene and Tropical Medicine, London, United Kingdom;School of Molecular Medical Sciences, Centre for Biomolecular Science, University of Nottingham, Nottingham, United Kingdom

关键词: Biofilms;    Yersinia pseudotuberculosis;    Caenorhabditis elegans;    Bacterial biofilms;    Pathogen motility;    Secretion;    Nematode infections;    Regulator genes;   

DOI  :  10.1371/journal.ppat.1001250

学科分类：生物科学（综合）

来源: Public Library of Science

【 摘 要 】

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.

【 授权许可】

CC BY