THE ROLE OF CELL-CELL SIGNALING IN HOST COLONIZATION BY XYLELLA FASTIDIOSA

• Author(s): Lindow, Steven; Newman, Karyn; Purcell, Alexander;
• Abstract: Endophytic bacteria such as Xylella fastidiosa (Xf) colonize the internal tissues of the host, forming a structure very similar to a fixed biofilm inside the plant. Cells secrete extracellular polysaccharides that may serve to enhance surface attachment, to protect the cells from host defenses or to serve as a matrix to concentrate nutrient ions (Denny, 1995). But what happens when the local environment can no longer support further population growth? A key determinant of success for an endophyte is the ability to move within the plant, sending out scouts to colonize new areas within the host. For a xylem-restricted species such as Xf, movement must be from vessel to vessel, which would require degrading and traversing the pit membranes connecting them. We expect activities such as degradation of a pit membrane to be most successful when carried out by a community of cells since individual cells may be incapable of completing the feat on their own and may be detected and easily eliminated by the host. Therefore, cells must have a means by which to assess the size of their local population, and to coordinately regulate the expression of genes required for such processes only at the appropriate time. Our study aims to investigate cell-cell communication in Xf to determine its role in colonization and pathogenicity in grapevine. Xf shares sequence similarity with the plant pathogen s. Xanthomonas campestris pathovar campestris (Xcc). In Xcc, the expression of pathogenicity genes is controlled by the Rpf system of cell-cell communication, enabling a population of cells to launch a pathogenic attack in a coordinated manner (Barber et al., 1997). The rpf (regulation of pathogenicity factors) genes of Xcc encode the components of a cell-cell communication system. Two of the Rpf proteins work to produce a diffusible signal factor (DSF; Barber et al., 1997). As the population grows, the local concentration of DSF increases. Other Rpf proteins are thought to sense the increase in DSF concentration and transduce a signal, resulting in expression of pathogenicity factors (Slater et al., 2000). The Xf genome not only contains homologs of the rpf genes most essential for cell-cell signaling in Xcc, but also exhibits striking colinearity in the arrangement of these genes on the chromosome. Furthermore, the Xf genome lacks homologs of the luxI/luxR genes and other genes shown to be involved in production and perception of AHLs (Dow and Daniels, 2000). Thus it is likely that Xf employs a cell-cell signaling apparatus similar to that of Xcc. Based on our knowledge of density-dependent gene regulation in other species, we predict the targets of Rpf regulation would be genes necessary for colonizing the xylem and spreading from vessel to vessel. For example, expression of extracellular polysaccharides, cellulases, proteases and pectinases might be induced by the signal. Similarly, we would expect the density-dependent genes to be expressed during the time when a population of Xf is ready to move into uncolonized areas of the plant.It is conceivable that cell-cell signal interference may be used by other organisms to inhibit density-dependent behaviors, such as pathogenicity or spreading through the habitat. Several recent studies indicate that other organisms can disrupt or manipulate the cell-cell signaling system of bacteria (Leadbetter and Greenberg, 2000; Manefield et al., 1999). Examination of Xf population size in plants where Xf lives as an endophyte versus those in which Xf causes the xylem blockage symptoms of Pierces disease demonstrates a positive relationship between population size and symptom development (Fry and Milholland, 1990). We hypothesize that an interaction between Xf and other organisms, such as another endophyte or the host plant itself, may modulate density-dependent behaviors in Xf by interfering with cell-cell signaling.
• Publication Date: Dec 2001
• Journal: 2001 Pierce's Disease Research Symposium