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Journal of Bacteriology, October 2004, p. 6837-6844, Vol. 186, No. 20
0021-9193/04/$08.00+0     DOI: 10.1128/JB.186.20.6837-6844.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

The Transcriptional Regulator AlgR Controls Cyanide Production in Pseudomonas aeruginosa

Alexander J. Carterson,1 Lisa A. Morici,1 Debra W. Jackson,1 Anders Frisk,1 Stephen E. Lizewski,1 Ryan Jupiter,1 Kendra Simpson,1 Daniel A. Kunz,2 Scott H. Davis,3 Jill R. Schurr,4 Daniel J. Hassett,5 and Michael J. Schurr1*

Department of Microbiology and Immunology, Program in Molecular Pathogenesis and Immunity, Louisiana Center for Lung Biology and Immunotherapy,1 Department of Pediatrics, Tulane University Health Sciences Center,3 Department of Genetics, Louisiana State University Health Sciences Center, New Orleans, Louisiana,4 Division of Biochemistry and Molecular Biology, Department of Biological Sciences, University of North Texas, Denton, Texas,2 Department of Molecular Genetics, Biochemistry, and Microbiology, University of Cincinnati College of Medicine, Cincinnati, Ohio5

Received 27 April 2004/ Accepted 14 July 2004

Pseudomonas aeruginosa is an opportunistic pathogen that causes chronic lung infections in cystic fibrosis (CF) patients. One characteristic of P. aeruginosa CF isolates is the overproduction of the exopolysaccharide alginate, controlled by AlgR. Transcriptional profiling analyses comparing mucoid P. aeruginosa strains to their isogenic algR deletion strains showed that the transcription of cyanide-synthesizing genes (hcnAB) was ~3-fold lower in the algR mutants. S1 nuclease protection assays corroborated these findings, indicating that AlgR activates hcnA transcription in mucoid P. aeruginosa. Quantification of hydrogen cyanide (HCN) production from laboratory isolates revealed that mucoid laboratory strains made sevenfold more HCN than their nonmucoid parental strains. In addition, comparison of laboratory and clinically derived nonmucoid strains revealed that HCN was fivefold higher in the nonmucoid CF isolates. Moreover, the average amount of cyanide produced by mucoid clinical isolates was 4.7 ± 0.85 µmol of HCN/mg of protein versus 2.4 ± 0.40 µmol of HCN/mg of protein for nonmucoid strains from a survey conducted with 41 P. aeruginosa CF isolates from 24 patients. Our data indicate that (i) mucoid P. aeruginosa regardless of their origin (laboratory or clinically derived) produce more cyanide than their nonmucoid counterparts, (ii) AlgR regulates HCN production in P. aeruginosa, and (iii) P. aeruginosa CF isolates are more hypercyanogenic than nonmucoid laboratory strains. Taken together, cyanide production may be a relevant virulence factor in CF lung disease, the production of which is regulated, in part, by AlgR.

* Corresponding author. Mailing address: Department of Microbiology and Immunology, Tulane University Health Sciences Center, 1430 Tulane Ave., New Orleans, LA 70112-2699. Phone: (504) 988-4607. Fax: (504) 588-5144. E-mail: mschurr{at}tulane.edu.

Journal of Bacteriology, October 2004, p. 6837-6844, Vol. 186, No. 20
0021-9193/04/$08.00+0     DOI: 10.1128/JB.186.20.6837-6844.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.



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