The Transcriptional Regulator AlgR Controls Cyanide Production in
            <i>Pseudomonas aeruginosa</i>

Carterson, Alexander J.; Morici, Lisa A.; Jackson, Debra; Frisk, Anders; Lizewski, Stephen E.; Jupiter, Ryan; Simpson, Kendra; Kunz, Daniel A.; Davis, Scott H.; Schurr, Jill R.; Hassett, Daniel J.; Schurr, Michael J.

doi:10.1128/jb.186.20.6837-6844.2004

Cited by 75 publications

(83 citation statements)

References 57 publications

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“…In vitro data suggests that mucoid P. aeruginosa isolates produce more cyanide than nonmucoid laboratory strains [5], but such a relationship was not identified in the present study as all patients were colonised with mucoid strains (data not shown). Whether strains that produce more cyanide have a survival advantage in the CF lung environment or whether the alginate layer in mucoid strains simply increases cyanide output by limiting oxygen diffusion are questions that need to be examined further.…”

Section: Discussioncontrasting

confidence: 70%

“…In CF airways, P. aeruginosa is thought to grow in anaerobic/reduced oxygen pockets situated within thickened and tenacious mucus plugs that occlude small airways [3,4]. This environment may be suitable for cyanide production by P. aeruginosa [5][6][7]. However, to date, it is not known whether bacteria are residing in strictly anaerobic or microaerobic pockets within the CF lung.…”

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confidence: 99%

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Bacterial cyanogenesis occurs in the cystic fibrosis lung

Sanderson¹,

Wescombe²,

Kirov³

et al. 2008

European Respiratory Journal

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The cystic fibrosis (CF) lung environment is poorly defined, but data suggest that bacteria may encounter reduced oxygen tensions and possibly an anaerobic environment. Pseudomonas aeruginosa produces the potent toxin cyanide under strictly microaerobic conditions. Evidence of bacterial cyanogenesis in the CF lung was investigated in the present study by measuring sputum cyanide concentrations.Sputum cyanide was measured in seven stable CF patients, as well as before and after intravenous antibiotic therapy during a hospital admission in a further eight patients experiencing acute exacerbations. All patients were chronically infected with P. aeruginosa. Comparative sputum data were obtained from nine CF patients with no documented P. aeruginosa infection and 10 healthy, nonsmoking normal controls.High levels of cyanide were detected in all the P. aeruginosa-infected stable CF patients (median (range) 0.56 (0.37-2.81) mg?mL -1 ), and in seven out of eight acute sputum samples (0.73 (0-1.43) mg?mL -1 ). In contrast, cyanide was not detectable in sputum from eight out of nine CF patients without P. aeruginosa infection or in any of the normal controls. Intravenous antibiotic treatment significantly reduced sputum cyanide levels (median 0.73 to median 0.0 mg?mL -1 ).The cyanide detected indicates that the cystic fibrosis lung provides a predominantly microaerobic environment for Pseudomonas aeruginosa. Cyanide is likely to be a potentially important virulence factor in Pseudomonas aeruginosa-infected cystic fibrosis patients.

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Section: Discussioncontrasting

confidence: 70%

mentioning

confidence: 99%

Bacterial cyanogenesis occurs in the cystic fibrosis lung

Sanderson¹,

Wescombe²,

Kirov³

et al. 2008

European Respiratory Journal

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“…It has been described that clinical isolates of P. aeruginosa produced high levels of cyanide (22) as a secondary metabolite (23) and that cyanide can be a relevant determinant for the virulence of P. aeruginosa in wounds from burn patients (24) as well as in lung infections of CF patients (22). Because cyanide has also been described as a relevant element in the infectiondriven killing of C. elegans by P. aeruginosa (25), we have analyzed the effect of this compound in the physiology of the wild-type and the evolved C. elegans strains.…”

Section: Resultsmentioning

confidence: 99%

Experimental validation of Haldane's hypothesis on the role of infection as an evolutionary force for Metazoans

Navas

Cobas

Talavera

et al. 2007

Proc. Natl. Acad. Sci. U.S.A.

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A common drawback in evolutionary science is the fact that the evolution of organisms occurs in geological timing, completely out of the time scale of laboratory experimental work. For this reason, some relevant hypotheses on evolution of Metazoans are based on correlations more than on experimental data obtained for testing the robustness of those hypotheses. In the current work, we implement an experimental methodology to analyze the role of infections as a driving force in the evolution of Metazoans (Haldane's hypothesis). To that goal, we have used simple models of virulence with short reproduction times, large populations, and that are easily testable in the laboratory. Using the bacteriovirus nematode Caenorhabditis elegans as a model organism under evolution and their infection by the environmental opportunistic bacterial pathogen Pseudomonas aeruginosa as the selective force, we have demonstrated that bacterial infection selects an evolved nematode lineage resistant to infection, with changes in its respiration and capability of consuming novel food resources. Using an experimental approach, we show that infection is a selective force in the evolution of Metazoans as proposed earlier by Haldane.Pseudomonas aeruginosa ͉ Caenorhabditis elegans ͉ opportunistic pathogens ͉ experimental evolution

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“…AlgR regulates the hcnABC operon genes (PA2193-PA2195) involved in hydrogen cyanide synthesis in P. aeruginosa (480). In the ampR mutant, these genes are downregulated five-to seven-fold without a corresponding significant differential regulation of algR (< two-fold).…”

Section: Phenotypic Microarray Analysis Of Pao∆amprmentioning

confidence: 99%

“…In addition to regulating the algD operon, AlgR directly activates transcription of algC (PA5322), which encodes a phosphomannomutase/phosphoglucomutase essential for Psl, alginate and rhamnolipid synthesis ( Figure 6.2) (739-742). AlgR also is important for mature biofilm formation, possibly by directly repressing rhl-QS (743), type IV pilus formation by binding to the fimTU-pilVWXY1Y2E promoter (744,745), and hydrogen cyanide (HCN) production by binding to the hcnA (PA2193) promoter (480). Interestingly, in contrast to alginate production, the phosphorylation site is required for regulating cyanide production and twitching motility (744,746).…”

Section: Alginate Productionmentioning

confidence: 99%

Pseudomonas Aeruginosa AmpR Transcriptional Regulatory Network

Balasubramanian¹

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The Transcriptional Regulator AlgR Controls Cyanide Production in Pseudomonas aeruginosa

Cited by 75 publications

References 57 publications

Bacterial cyanogenesis occurs in the cystic fibrosis lung

Bacterial cyanogenesis occurs in the cystic fibrosis lung

Experimental validation of Haldane's hypothesis on the role of infection as an evolutionary force for Metazoans

Pseudomonas Aeruginosa AmpR Transcriptional Regulatory Network

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