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Journal of Bacteriology, March 1999, p. 1623-1629, Vol. 181, No. 5
0021-9193/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.
Roles of Pseudomonas aeruginosa las and
rhl Quorum-Sensing Systems in Control of Twitching
Motility
Alex
Glessner,1
Roger S.
Smith,2
Barbara H.
Iglewski,2 and
Jayne
B.
Robinson1,*
Department of Biology, University of Dayton,
Dayton, Ohio 45469,1 and Department of
Microbiology and Immunology, University of Rochester School of Medicine
and Dentistry, Rochester, New York 146422
Received 27 August 1998/Accepted 17 December 1998
Pseudomonas aeruginosa is a ubiquitous environmental
bacterium and an important human pathogen. The production of several virulence factors by P. aeruginosa is controlled through
two quorum-sensing systems, las and rhl. We
have obtained evidence that both the las and
rhl quorum-sensing systems are also required for type 4 pilus-dependent twitching motility and infection by the pilus-specific phage D3112cts. Mutants which lack the ability to
synthesize PAI-1, PAI-2, or both autoinducers were significantly or
greatly impaired in twitching motility and in susceptibility to
D3112cts. Twitching motility and phage susceptibility in
the autoinducer-deficient mutants were partially restored by exposure
to exogenous PAI-1 and PAI-2. Both twitching motility and infection by
pilus-specific phage are believed to be dependent on the extension and
retraction of polar type 4 pili. Western blot analysis of whole-cell
lysates and enzyme-linked immunosorbent assays of intact cells were
used to measure the amounts of pilin on the cell surfaces of
las and rhl mutants relative to that of the
wild type. It appears that PAI-2 plays a crucial role in twitching
motility and phage infection by affecting the export and assembly of
surface type 4 pili. The ability of P. aeruginosa cells to
adhere to human bronchial epithelial cells was also found to be
dependent on the rhl quorum-sensing system. Microscopic
analysis of twitching motility indicated that mutants which were unable
to synthesize PAI-1 were defective in the maintenance of cellular
monolayers and migrating packs of cells. Thus, PAI-1 appears to have an
essential role in maintaining cell-cell spacing and associations
required for effective twitching motility.
*
Corresponding author. Mailing address: Department of
Biology, University of Dayton, 300 College Park, Dayton, OH 45469-2320. Phone: (937) 229-2580. Fax: (937) 229-2021. E-mail:
robinson{at}neelix.udayton.edu.
Journal of Bacteriology, March 1999, p. 1623-1629, Vol. 181, No. 5
0021-9193/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.
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