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Journal of Bacteriology, February 2003, p. 1071-1081, Vol. 185, No. 3
0021-9193/03/$08.00+0     DOI: 10.1128/JB.185.3.1071-1081.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.

Microarray Analysis of Global Gene Expression in Mucoid Pseudomonas aeruginosa

Aaron M. Firoved1 and Vojo Deretic2*

Department of Microbiology and Immunology, University of Michigan Medical School, Ann Arbor, Michigan 48109-0620,1 Department of Molecular Genetics and Microbiology, University of New Mexico Health Sciences Center, Albuquerque, New Mexico 871312

Received 19 July 2002/ Accepted 1 November 2002

Pseudomonas aeruginosa is the dominant pathogen causing chronic respiratory infections in cystic fibrosis (CF). After an initial phase characterized by intermittent infections, a chronic colonization is established in CF upon the conversion of P. aeruginosa to the mucoid, exopolysaccharide alginate-overproducing phenotype. The emergence of mucoid P. aeruginosa in CF is associated with respiratory decline and poor prognosis. The switch to mucoidy in most CF isolates is caused by mutations in the mucA gene encoding an anti-sigma factor. The mutations in mucA result in the activation of the alternative sigma factor AlgU, the P. aeruginosa ortholog of Escherichia coli extreme stress sigma factor {sigma}E. Because of the global nature of the regulators of mucoidy, we have hypothesized that other genes, in addition to those specific for alginate production, must be induced upon conversion to mucoidy, and their production may contribute to the pathogenesis in CF. Here we applied microarray analysis to identify on the whole-genome scale those genes that are coinduced with the AlgU sigmulon upon conversion to mucoidy. Gene expression profiles of AlgU-dependent conversion to mucoidy revealed coinduction of a specific subset of known virulence determinants (the major protease elastase gene, alkaline metalloproteinase gene aprA, and the protease secretion factor genes aprE and aprF) or toxic factors (cyanide synthase) that may have implications for disease in CF. Analysis of promoter regions of the most highly induced genes (>40-fold, P <= 10-4) revealed a previously unrecognized, putative AlgU promoter upstream of the osmotically inducible gene osmE. This newly identified AlgU-dependent promoter of osmE was confirmed by mapping the mRNA 5' end by primer extension. The recognition of genes induced in mucoid P. aeruginosa, other than those associated with alginate biosynthesis, reported here revealed the identity of previously unappreciated factors potentially contributing to the morbidity and mortality caused by mucoid P. aeruginosa in CF.

* Corresponding author. Mailing address: Department of Molecular Genetics and Microbiology, University of New Mexico Health Sciences Center, 915 Camino de Salud, NE, Albuquerque, NM 87131. Phone: (505) 272-0291. Fax: (505) 272-6029. E-mail: vderetic{at}salud.unm.edu.

Journal of Bacteriology, February 2003, p. 1071-1081, Vol. 185, No. 3
0021-9193/03/$08.00+0     DOI: 10.1128/JB.185.3.1071-1081.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.



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