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Andrew P. Tomaras,1,
Adam P. Barker,1,#
Dennis R. Voelker,2
Edward D. Chan,2
Adriana I. Vasil,1 and
Michael L. Vasil1*
Department of Microbiology, University of Colorado—Denver, Aurora, Colorado 80045,1 Department of Medicine, National Jewish Medical and Research Center, Denver, Colorado 802062
Received 24 January 2008/ Accepted 24 March 2008
Pseudomonas aeruginosa demonstrates type IV pilus-mediated directional twitching motility up a gradient of phosphatidylethanolamine (PE). Only one of four extracellular phospholipases C of P. aeruginosa (i.e., PlcB), while not required for twitching motility per se, is required for twitching-mediated migration up a gradient of PE or phosphatidylcholine. Whether other lipid metabolism genes are associated with this behavior was assessed by analysis of transcription during twitching up a PE gradient in comparison to transcription during twitching in the absence of any externally applied phospholipid. Data support the hypothesis that PE is further degraded and that the long-chain fatty acid (LCFA) moieties of PE are completely metabolized via β-oxidation and the glyoxylate shunt. It was discovered that P. aeruginosa exhibits twitching-mediated chemotaxis toward unsaturated LCFAs (e.g., oleic acid), but not saturated LCFAs (e.g., stearic acid) of corresponding lengths. Analysis of mutants that are deficient in glyoxylate shunt enzymes, specifically isocitrate lyase (
aceA) and malate synthase (
aceB), suggested that the complete metabolism of LCFAs through this pathway was required for the migration of P. aeruginosa up a gradient of PE or unsaturated LCFAs. At this point, our data suggested that this process should be classified as energy taxis. However, further evaluation of the ability of the
aceA and
aceB mutants to migrate up a gradient of PE or unsaturated LCFAs in the presence of an alternative energy source clearly indicated that metabolism of LCFAs for energy is not required for chemotaxis toward these compounds.
Published ahead of print on 4 April 2008.
Supplemental material for this article may be found at http://jb.asm.org/.
These authors made equal contributions to this study.
# Present address: Microbiology and Molecular Genetics, Harvard Medical School, Warren Alpert Building, Rm. 352, 200 Longwood Ave., Boston, MA 02115.
| Appl. Environ. Microbiol. | Infect. Immun. | Eukaryot. Cell |
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| Mol. Cell. Biol. | J. Virol. | Microbiol. Mol. Biol. Rev. |
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