|BURCH, ADRIEN - University Of California|
|SHIMADA, BRIANA - University Of California|
|MULLIN, SEAN - University Of California|
|LINDOW, STEVEN - University Of California|
Submitted to: Journal of Bacteriology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 12/15/2011
Publication Date: 3/30/2012
Citation: Burch, A.Y., Shimada, B.K., Mullin, S.W., Dunlap, C.A., Bowman, M.J., Lindow, S.E. 2012. Pseudomonas syringae coordinates production of a motility-enabling surfactant with flagellar assembly. Journal of Bacteriology. 194(6):1287-1298.
Interpretive Summary: In this research, we identified an unknown metabolite produced by an important bacterial plant pathogen. This metabolite plays an important role in allowing the bacteria to colonize and move on plant surfaces. In addition, we identified the regulatory genes that control the metabolite’s production and identified some environmental conditions that induce the metabolite’s production. Understanding how bacteria use these compounds to colonize plant surfaces will allow us to develop improved strategies to control these plant pathogens. This research benefits farmers, scientists and crop protection companies with a better understanding of how bacterial plant pathogens colonize and infect plants.
Technical Abstract: Using a sensitive assay, we observed low levels of an unknown surfactant produced by Pseudomonas syringae pv. syringae B728a that was undetectable with traditional methods. Much larger quantities of this surfactant were produced by cells colonizing a porous hydrated paper surface than on agar surfaces. Random mutagenesis revealed an acyltransferase with homology to rhlA from P. aeruginosa that was required for production of this surfactant, identified by mass spectrometry as HAA. Analysis of other mutants altered in surfactant production revealed that HAA is coordinately regulated with the late-stage flagellar gene encoding flagellin; mutations in genes involved in early flagellar assembly abolish or reduce HAA production, while mutations in flagellin or flagellin glycosylation genes increase its production. When colonizing a rough porous surface, the bacterium increases production of both flagellin and HAA. P. syringae was defective in porous paper colonization without functional flagella, and was slightly inhibited in its movement when it lacked HAA production. In contrast, loss of HAA production had no effect on swimming but abolished swarming motility. A strain that lacked HAA but produced syringafactin exhibited broad swarming tendrils, while a strain that overproduced HAA exhibited slender swarming tendrils. Based on further analysis of mutants altered in HAA production, we propose a model of its regulation in Pseudomonas syringae B728a.