DSF signalling and biofilm formation in Xanthomonas campestris

J. MAX DOW; M. R. MARANO; A. A. VOJNOV

Portland, Oregon

Conferencia; 2009 American Phytopathological Society Annual Meeting; 2009

American Phytopathological Society (APS)

Xanthomonas campestris pathovar campestris (Xcc) is the causal agent of black rot of crucifers. The ability of Xcc to incite disease depends on cell-cell signaling involving the diffusible factor DSF. The synthesis of DSF depends upon RpfF and perception and signal transduction involves the RpfC/RpfG two-component system. Mutations in rpfC lead to DSF over-production. In certain liquid media, rpfF, rpfG and rpfC mutants grow as large multicellular aggregates rather than the dispersed planktonic form of the wild type. Addition of DSF causes dispersal of aggregates formed by rpfF strains but not rpfG or rpfC strains. Strains carrying additional mutations in gumB, which is required for biosynthesis of xanthan, are unable to form aggregates indicating that this polysaccharide is a component of the bacterial matrix. In minimal medium without shaking a different picture emerges. Wildtype Xcc forms microcolonies that develop into a structured biofilm, whereas rpfF and rpfC mutants form only unstructured arrangements of bacteria. A gumB mutant is unable to develop the typical wildtype biofilm. Mixed cultures of gumB and rpfF mutants form a typical biofilm; in contrast, the rpfC mutant prevents the formation of the structured biofilm by the wildtype. These findings suggest that DSF signaling is finely balanced during biofilm formation.