Abstract
Burkholderia glumae is a plant pathogenic bacterium that uses an acyl-homoserine lactone-mediated quorum sensing system to regulate protein secretion, oxalate production and major virulence determinants such as toxoflavin and flagella. B. glumae also releases surface-active rhamnolipids. In Pseudomonas aeruginosa and Burkholderia thailandensis, rhamnolipids, along with flagella, are required for the social behavior called swarming motility. In the present study, we demonstrate that quorum sensing positively regulates the production of rhamnolipids in B. glumae and that rhamnolipids are necessary for swarming motility also in this species. We show that a rhlA- mutant, which is unable to produce rhamnolipids, loses its ability to swarm, and that this can be complemented by providing exogenous rhamnolipids. Impaired rhamnolipid production in a quorum sensing-deficient B. glumae mutant is the main factor responsible for its defective swarming motility behaviour.
Highlights
Burkholderia glumae is a notorious phytopathogen of rice that uses a LuxI/LuxR-type quorum sensing (QS) system to regulate diverse cellular processes such as protein secretion, oxalate production and expression of major known virulence factors, including toxoflavin, lipase, KatG and flagella [1,2,3,4]
We have previously reported that B. glumae is capable of rhamnolipids production and carries a rhl operon homologous to those responsible for rhamnolipid biosynthesis in B. thailandensis, Burkholderia pseudomallei and P. aeruginosa [13]
Rhamnolipid production is necessary for B. glumae swarming motility
Summary
Burkholderia glumae is a notorious phytopathogen of rice that uses a LuxI/LuxR-type quorum sensing (QS) system to regulate diverse cellular processes such as protein secretion, oxalate production and expression of major known virulence factors, including toxoflavin, lipase, KatG and flagella [1,2,3,4]. Among major virulence determinants of B. glumae, flagellum-driven motility plays a critical role in its pathogenicity [1]. Besides swimming motility, this bacterium is able to spread by a social motility behaviour called swarming motility, which typically requires both functional flagella and production of a surface-wetting agent (surfactant) [6]. QS modulates swarming motility by diverse mechanisms, either by regulating the flagellar machinery and propulsive force, or by inducing the expression of wetting agent biosynthesis pathways [8]. In B. glumae, QS positively regulates the expression of flagellar biosynthesis genes, which are essential for swarming motility [1].
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