Pseudomonas aeruginosa PA1006, which plays a role in molybdenum homeostasis, is required for nitrate utilization, biofilm formation, and virulence

• Published in: PloS one 2013-02, Vol.8 (2), p.e55594-e55594
• Main Authors: Filiatrault, Melanie J, Tombline, Gregory, Wagner, Victoria E, Van Alst, Nadine, Rumbaugh, Kendra, Sokol, Pam, Schwingel, Johanna, Iglewski, Barbara H
• Format: Article
• Language: English
• Subjects: Analysis; Bacterial Proteins - genetics; Bacterial Proteins - physiology; Biofilms; Biology; Biosynthesis; Chemical bonds; Continuous flow; Cystic fibrosis; Dentistry; DNA microarrays; E coli; Enzymes; Escherichia coli; Flow system; Gene expression; Genes; Homeostasis; Homology; Immunology; Intermediates; Iron; Iron and steel making; Kinases; Laboratories; Lungs; Medicine; Metabolism; Molybdenum; Molybdenum - metabolism; Nitrate reductase; Nitrates; Nitrates - metabolism; Nitric oxide; Nosocomial infections; Oligonucleotide Array Sequence Analysis; Opportunist infection; Physiological aspects; Proteins; Pseudomonas aeruginosa; Pseudomonas aeruginosa - metabolism; Pseudomonas aeruginosa - pathogenicity; Quorum sensing; Secretion; Sulfur; Tricarboxylic acid cycle; Virulence
• ISSN: 1932-6203; 1932-6203
• DOI: 10.1371/journal.pone.0055594

Pseudomonas aeruginosa (Pae) is a clinically important opportunistic pathogen. Herein, we demonstrate that the PA1006 protein is critical for all nitrate reductase activities, growth as a biofilm in a continuous flow system, as well as virulence in mouse burn and rat lung model systems. Microarray analysis revealed that ΔPA1006 cells displayed extensive alterations in gene expression including nitrate-responsive, quorum sensing (including PQS production), and iron-regulated genes, as well as molybdenum cofactor and Fe-S cluster biosynthesis factors, members of the TCA cycle, and Type VI Secretion System components. Phenotype Microarray™ profiles of ΔPA1006 aerobic cultures using Biolog plates also revealed a reduced ability to utilize a number of TCA cycle intermediates as well as a failure to utilize xanthine as a sole source of nitrogen. As a whole, these data indicate that the loss of PA1006 confers extensive changes in Pae metabolism. Based upon homology of PA1006 to the E. coli YhhP protein and data from the accompanying study, loss of PA1006 persulfuration and/or molybdenum homeostasis are likely the cause of extensive metabolic alterations that impact biofilm development and virulence in the ΔPA1006 mutant.