Study of flagella-mediated interactions between plants and Pseudomonas syringae

Abstract

The phytopathogenic bacterium P. syringae can be classified into more than 50 pathovars on the basis of their host plant species and the disease symptoms they cause. They enter apoplastic spaces of host plants via natural openings such as wounds and stomata in leaves, stems, and fruits, then multiply and cause leaf spots, necrosis, wilt and stem canker. Each P. syringae pathovar has its own host species. For example, P. syringae pv. tabaci (Pta) 6605 is the causal agent of wild fire disease in tobacco, but does not cause disease in nonhost plants such as tomato and Arabidopsis thaliana. In Gram-negative phytopathogenic bacteria, a hrp (hypersensitive reaction and pathogenicity) gene cluster is required to cause the hypersensitive reaction (HR) on nonhost plants and pathogenicity on host plants. The hrp gene cluster encodes components of the Hrp type III secretion apparatus, regulatory proteins for hrp gene expression and the harpin protein, a proteinaceous elicitor effective on nonhost plants. Harpin is encoded by hrpZ in the hrp gene cluster. We have investigated the hrpZ gene in several pathovars of P. syringae and revealed that hrpZ in strain Pta6605 has a deleterious internal deletion and frame shift, and thus does not produce active elicitor. Harpin is thought to be a major elicitor of HR in nonhost plants, and we predicted that Pta6605 has a different elicitor because Pta6605 does induce typical HR on nonhost tomato plants. By screening for active elicitor molecules in the culture supernatant of Pta6605, we identified the flagellin protein, a major component of the flagellar filament, as a strong elicitor of hypersensitive cell death in tomato.