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Pseudomonas syringae elicits a variety of symptoms on plants, including cankers, leaf spots, and galls, and is divided into pathogenic variants (pathovars; pv.) that vary in host range. The infection of host plants by P syringae is a multi-step process involving epiphytic (surface) colonization, entry, establishment of infection sites in the apoplast (intercellular spaces), multiplication to high levels within host tissue, and production of disease syrnptoms5. The genetic basis of pathogenicity in P syringae includes global regulatory loci56, 108, the hrp/hrc cluster, phytotoxins, exopolysaccharides, and other virulence factors5, 10, 19, 54. The hrp/hrc genes encode a type III secretion system (TTSS), which is functionally similar to the TTSS identified in Gramnegative animal pathogens38. In P syringae, the TTSS is required for growth in susceptible host plants and the activation of plant defense in nonhost plants; the latter is often associated with the hypersensitive response (HR)123. Although the TTSS is the best described virulence system for P. syringae, it is not the only component required for establishment ofa successful infection5, 54. |
