Jpn. J. Infect. Dis., 65 (2), 126-131, 2012
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Tetsuyoshi Inoue1, Teruo Kuroda2, and Naoya Ohara1*
1Department of Oral Microbiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University, Okayama 700-8525 and 2Department of Genome Applied Microbiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University, Okayama 700-8530, Japan
(Received September 13, 2011. Accepted December 6, 2011)
*Corresponding author: Mailing address: Department of Oral Microbiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University, Shikata, Okayama 700-8525, Japan. Tel: +81-86-235-6655, Fax: +81-86-235-6659, E-mail: このメールアドレスはスパムボットから保護されています。閲覧するにはJavaScriptを有効にする必要があります。
SUMMARY: Pseudomonas aeruginosa is known to produce surfactants that are involved in its swarming motility behavior, such as rhamnolipids and their precursors―3-(3-hydroxyalkanoyloxy)-alkanoic acids (HAAs). In P. aeruginosa PAO1, swarming motility is inhibited by some fatty acids, including branched-chain fatty acids and unsaturated fatty acids. In the present study, addition of 12-methyltetradecanoic acid (12-MTA, anteiso-C15:0) to an agar medium markedly repressed surfactant activity in the extracellular fraction of a P. aeruginosa culture in a drop collapse assay. Further, an extracellular fraction of a culture of rhlA mutant P. aeruginosa, which did not produce both rhamnolipids and HAAs, showed a complete loss of surfactant activity and markedly reduced swarming activity. In contrast, an extracellular fraction of a culture of rhlB mutant P. aeruginosa, which produced HAAs but not rhamnolipids, showed moderate swarming activity and weak extracellular surfactant activity that was lost on the addition of 12-MTA to the agar medium. Expression of the rhlAB operon from the plasmid pMR2 restored normal swarming motility on 12-MTA-containing agar medium. Taken together, these findings indicate that 12-MTA reduced extracellular surfactant activity, thus resulting in a swarming defect in P. aeruginosa PAO1.
