Journal of Bacteriology, May 2004, p. 2936-2945, Vol. 186, No. 10
0021-9193/04/$08.00+0 DOI: 10.1128/JB.186.10.2936-2945.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.
Positive Control of Swarming, Rhamnolipid Synthesis, and Lipase Production by the Posttranscriptional RsmA/RsmZ System in Pseudomonas aeruginosa PAO1
Karin Heurlier,1 Faye Williams,2,3 Stephan Heeb,1,2 Corinne Dormond,1 Gabriella Pessi,1,
Dustin Singer,1 Miguel Cámara,2,3 Paul Williams,2,3 and Dieter Haas1*
Institut de Microbiologie Fondamentale, Université de Lausanne, CH-1015 Lausanne, Switzerland,1
Institute of Infection, Immunity, and Inflammation, University of Nottingham, Queen's Medical Centre, Nottingham NG7 2UH,2
School of Pharmaceutical Sciences, University of Nottingham, University Park, Nottingham NG7 2RD, United Kingdom3
Received 13 August 2003/
Accepted 4 February 2004
In Pseudomonas aeruginosa, the small RNA-binding, regulatory protein RsmA is a negative control element in the formation of several extracellular products (e.g., pyocyanin, hydrogen cyanide, PA-IL lectin) as well as in the production of N-acylhomoserine lactone quorum-sensing signal molecules. RsmA was found to control positively the ability to swarm and to produce extracellular rhamnolipids and lipase, i.e., functions contributing to niche colonization by P. aeruginosa. An rsmA null mutant was entirely devoid of swarming but produced detectable amounts of rhamnolipids, suggesting that factors in addition to rhamnolipids influence the swarming ability of P. aeruginosa. A small regulatory RNA, rsmZ, which antagonized the effects of RsmA, was identified in P. aeruginosa. Expression of the rsmZ gene was dependent on both the global regulator GacA and RsmA, increased with cell density, and was subject to negative autoregulation. Overexpression of rsmZ and a null mutation in rsmA resulted in quantitatively similar, negative or positive effects on target genes, in agreement with a model that postulates titration of RsmA protein by RsmZ RNA.
* Corresponding author. Mailing address: Institut de Microbiologie Fondamentale, BÂtiment de Biologie, Université de Lausanne, CH-1015 Lausanne Dorigny, Switzerland. Phone: 41 21 6925631. Fax: 41 21 6925635. E-mail: Dieter.Haas{at}imf.unil.ch.
This work is dedicated to the memory of Faye Williams who was an ever-smiling collaborator in this project. She died tragically on 14 November 2001.
Present address: Department of Genetics and Developmental Biology, Center for Microbial Pathogenesis, University of Connecticut Health Center, Farmington, CT 06030-3710.
Journal of Bacteriology, May 2004, p. 2936-2945, Vol. 186, No. 10
0021-9193/04/$08.00+0 DOI: 10.1128/JB.186.10.2936-2945.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.
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Copyright © 2004 by the American Society for Microbiology. All rights reserved.