Pathogenicity and virulence factors of Pseudomonas syringae

Abstract

In 1994, Oku reported that plant pathogens, mainly fungal pathogens, require three essential abilities to infect plants: to enter plants, to overcome host resistance, and to evoke disease. Because the infectious process of phytopathogenic bacteria differs from that of fungal pathogens, we have attempted to characterize pathogenicity, the ability of a pathogen to cause disease, using the phytopathogenic bacterium Pseudomonas syringae as a representative pathogen. To establish infection and incite disease development, bacteria first have to enter a plant. This process requires flagella- and type IV pili-mediated motility, and active taxis is probably necessary for effective infection. After bacteria enter a plant’s apoplastic spaces, they need to overcome host plant resistance. To do this, they secrete a wide variety of hypersensitive response and pathogenicity (Hrp) effector proteins into the plant cytoplasm to interfere with pathogen/microbe-associated molecular pattern- and effector-triggered immunity, produce phytohormones and/or phytotoxins to suppress plant defense responses and extracellular polysaccharides to prevent access by antibiotics and to chelate Ca2+, and activate the multidrug resistance efflux pump to extrude antimicrobial compounds for successful colonization. Furthermore, to evoke disease, bacteria produce toxins and Hrp effectors that compromise a plant’s homeostasis and injure plant cells. The expression of these virulence factors depends on the infection processes and environmental conditions. Thus, the expression and function of virulence factors interact with each other, creating complex networks in the regulation of bacterial virulence-related genes.