Abstract
Burkholderia gladioli produces a yellow-pigmented toxin called toxoflavin, and causes disease on a variety of plants. Previous studies have suggested that the pathogenicity of B. gladioli is regulated by an N-acyl-l-homoserine lactone (AHL)-mediated quorum sensing (QS) system. In this study, complete genome sequencing revealed that B. gladioli pv. gladioli MAFF 302385 possesses two types of AHL synthase and AHL receptor gene pairs: glaI1/glaR1 and glaI2/glaR2. Disruption of QS genes revealed that the glaI1/glaR1 QS system regulated swarming motility, biofilm formation, and colony formation via N-octanoyl-l-homoserine lactone. Although Escherichia coli harboring glaI2 produced N-(3-hydroxyoctanoyl)-l-homoserine lactone and N-(3-hydroxydecanoyl)-l-homoserine lactone, the expression of glaI2 was not confirmed in MAFF 302385 cells. We also found that toxoflavin production was regulated by the glaI1/glaR1 QS system in liquid medium, but not on agar medium. When pathogenicity tests were performed on gladiolus leaves, the wild-type and QS mutants showed a similar level of disease. Our results demonstrated that only the glaI1/glaR1-mediated QS system is active in MAFF 302385, but major virulence factors, especially toxoflavin, are not completely dependent on the QS system.