A Caenorhabditis elegans model of Yersinia infection: biofilm formation on a biotic surface

Abstract

To investigateYersiniapathogenicity and the evolutionary divergence of the genus, the effect of pathogenic yersiniae on the model organismCaenorhabditis eleganswas studied. Three strains ofYersinia pestis, including a strain lacking pMT1, caused blockage and death ofC. elegans; one strain, lacking the haemin storage (hms) locus, caused no effect. Similarly, 15 strains ofYersinia enterocoliticacaused no effect. Strains ofYersinia pseudotuberculosisshowed different levels of pathogenicity. The majority of strains (76 %) caused no discernible effect; 5 % caused a weak infection, 9·5 % an intermediate infection, and 9·5 % a severe infection. There was no consistent relationship between serotype and severity of infection; nor was there any relationship between strains causing infection ofC. elegansand those able to form a biofilm on an abiotic surface. Electron microscope and cytochemical examination of infected worms indicated that the infection phenotype is a result of biofilm formation on the head of the worm. Seven transposon mutants ofY. pseudotuberculosisstrain YPIII pIB1 were completely or partially attenuated; mutated genes included genes encoding proteins involved in haemin storage and lipopolysaccharide biosynthesis. A screen of 15 definedC. elegansmutants identified four where mutation caused (complete) resistance to infection byY. pseudotuberculosisYPIII pIB1. These mutants,srf-2,srf-3,srf-5and the dauer pathway genedaf-1, also exhibit altered binding of lectins to the nematode surface. This suggests that biofilm formation on a biotic surface is an interactive process involving both bacterial and invertebrate control mechanisms.