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Pseudomonas syringae pv. tabaci 6605 causes wildfire disease on host tobacco plants. To investigate the regulatory mechanism of the expression of virulence, Gac two-component system-defective mutants, !gacA and !gacS, and a double mutant, !gacA!gacS, were generated. These mutants produced smaller amounts of N-acyl homoserine lactones, required for quorum sensing, had lost swarming motility, and had reduced expression of virulence-related hrp genes and the algT gene required for exopolysaccharide production.The ability of the mutants to cause disease symptoms in their host tobacco plant was remarkably reduced, while they retained the ability to induce hypersensitive reaction (HR) in non-host plants. These results indicated that the Gac two-component system of P. syringae pv.tabaci 6605 is indispensable for virulence on the host plant, but not for HR induction in non-host plants.Marutani et al.,

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