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Journal of Bacteriology, December 2002, p. 6481-6489, Vol. 184, No. 23
0021-9193/02/$04.00+0     DOI: 10.1128/JB.184.23.6481-6489.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.

Autolysis and Autoaggregation in Pseudomonas aeruginosa Colony Morphology Mutants

David A. D'Argenio,1* M. Worth Calfee,2 Paul B. Rainey,3 and Everett C. Pesci2

Department of Genome Sciences, University of Washington, Seattle, Washington 98195-7730,1 Department of Microbiology and Immunology, East Carolina University School of Medicine, Greenville, North Carolina 27858,2 Department of Plant Sciences, University of Oxford, Oxford OX1 3RB, United Kingdom3

Received 22 May 2002/ Accepted 9 August 2002

Two distinctive colony morphologies were noted in a collection of Pseudomonas aeruginosa transposon insertion mutants. One set of mutants formed wrinkled colonies of autoaggregating cells. Suppressor analysis of a subset of these mutants showed that this was due to the action of the regulator WspR and linked this regulator (and the chemosensory pathway to which it belongs) to genes that encode a putative fimbrial adhesin required for biofilm formation. WspR homologs, related in part by a shared GGDEF domain, regulate cell surface factors, including aggregative fimbriae and exopolysaccharides, in diverse bacteria. The second set of distinctive insertion mutants formed colonies that lysed at their center. Strains with the most pronounced lysis overproduced the Pseudomonas quinolone signal (PQS), an extracellular signal that interacts with quorum sensing. Autolysis was suppressed by mutation of genes required for PQS biosynthesis, and in one suppressed mutant, autolysis was restored by addition of synthetic PQS. The mechanism of autolysis may involve activation of the endogenous prophage and phage-related pyocins in the genome of strain PAO1. The fact that PQS levels correlated with autolysis suggests a fine balance in natural populations of P. aeruginosa between survival of the many and persistence of the few.


* Corresponding author. Mailing address: Department of Microbiology, Health Sciences Building, K140, University of Washington, Box 357710, 1959 Pacific St. NE, Seattle, WA 98195-7710. Phone: (206) 221-5233. Fax: (206) 616-4295. E-mail: dargenio{at}u.washington.edu.


Journal of Bacteriology, December 2002, p. 6481-6489, Vol. 184, No. 23
0021-9193/02/$04.00+0     DOI: 10.1128/JB.184.23.6481-6489.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.




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