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PubMed1996

PhhR, a divergently transcribed activator of the phenylalanine hydroxylase gene cluster of Pseudomonas aeruginosa.

Pseudomonas aeruginosa was recently found to possess a cluster of structural genes encoding phenylalanine hydroxylase (PhhA), carbinolamine dehydratase (PhhB), and aromatic aminotransferase (PhhC). We now report the presence, in the flanking upstream region, of a divergently transcribed gene (phhR) encoding an activator protein. Inactivation of phhR markedly reduced expression of the structural genes. PhhR belongs to the large prokaryote family of sigma 54 enhancer-binding proteins, and activation of the phh operon by PhhR in P. aeruginosa required rpoN. The closest homologues of PhhR are the TyrR proteins from Escherichia coli and Haemophilus influenzae. E. coli TyrR is an unusual member of the homologue family in that the transcriptional units regulated by tyrR are driven by sigma 70 promoters. P. aeruginosa phhR was able to replace E. coli tyrR as a repressor of the aroF-tyrA operon (but not as an activator of mtr) in the heterologous E. coli system. Two regions that resemble E. coli TyrR boxes were identified in the intervening region between phhR and phhA. We propose that one or both boxes may be the target of PhhR acting as an autogenous repressor at a sigma 70 promoter in one direction. In the other direction, one or both boxes may be the upstream activator sequence targeted by PhhR to facilitate expression of the phh operon from a sigma 54 promoter. The phh operon was strongly induced in fructose- or glucose-based minimal medium by L-phenylalanine. Inactivation of phhR in P. aeruginosa abolished ability to utilize either L-phenylalanine or L-tyrosine as a sole source of carbon for growth.

Amino Acid Sequence↗

PubMed1994

Iron release from transferrin by pyoverdin and elastase from Pseudomonas aeruginosa.

Pseudomonas aeruginosa produces the siderophores pyoverdin and pyochelin as well as receptors for siderophores in response to iron deprivation. Previously, it has been shown in vitro that at neutral pH purified pyoverdin acquires iron from transferrin only in the presence of P. aeruginosa elastase (LasB), which proteolytically degrades transferrin. We constructed a LasB-negative mutant, PAO1E, by insertional mutagenesis to investigate whether this mutant differs in growth from the parental strain PAO1 in an iron-depleted medium supplemented with transferrin or human serum. PAO1 and PAO1E did not differ in growth with 1.25 microM Fe2-transferrin as the only iron source. Urea gel electrophoresis indicated iron release from intact transferrin during the logarithmic growth phase of PAO1 and PAO1E. A total of 333 microM LasB was synthesized from PAO1 after onset of stationary-phase growth. Quantification of pyoverdin by spectroscopy revealed that up to 900 microM pyroverdin was produced during growth of the strains in medium supplemented with Fe2-transferrin or 10% human serum. Incubation of Fe2-transferrin and purified pyoverdin in concentrations similar to those found in the culture supernatant resulted in release iron from transferrin after 10 h at 37 degrees C. However, LasB significantly enhanced the rate constant for iron acquisition of pyoverdin from transferrin. We conclude that P. aeruginosa can use transferrin as an iron source without further need of LasB or pH changes. This is further supported by experiments with P. aeruginosa K437, which has a defective iron uptake system, and its LasB-negative mutant, K437E. Though K437 and K437E did not differ in growth with Fe2-transferrin as the only iron source, their growth was significantly reduced relative to that of PAO1 and PAO1E.

Bacterial Proteins↗

PubMed1993

Cloning and sequence analysis of a gene (pchR) encoding an AraC family activator of pyochelin and ferripyochelin receptor synthesis in Pseudomonas aeruginosa.

Pseudomonas aeruginosa K372 is deficient in the production of both the 75-kDa ferripyochelin receptor protein and pyochelin. A 1.8-kb EcoRI-SalI fragment which restored production of both the receptor protein and pyochelin was cloned. Nucleotide sequencing of the fragment revealed an open reading frame of 888 bp, designated pchR (pyochelin), capable of encoding a 296-amino-acid protein of a 32,339-Da molecular mass. By using a phage T7-based expression system, a protein of ca. 32 kDa was produced off the 1.8-kb fragment, confirming that this open reading frame was indeed expressed. A region exhibiting homology to the consensus Fur-binding site of Escherichia coli was identified upstream of the pchR coding region overlapping a putative promoter. In addition, the C-terminal 80 amino acid residues of PchR showed approximately 50% homology (identity, 31%; conserved changes, 19%) to the carboxy terminus of AraC, a known transcriptional activator of gene expression in E. coli, Salmonella typhimurium, Citrobacter freundii, and Erwinia chrysanthemi. Within the C-terminal region of PchR, AraC, and a number of other members of the AraC family of transcriptional activators, there exists a highly conserved 17-residue domain where, in fact, two residues are strictly maintained and two others exhibit only conserved changes, suggesting a common functional significance to this region in all of these proteins. These data are consistent with a role for PchR as a transcriptional activator of pyochelin and ferripyochelin receptor synthesis in P. aeruginosa. In agreement with this, a PchR mutant obtained by in vitro mutagenesis and gene replacement was deficient in production of the ferripyochelin receptor and pyochelin.

Amino Acid Sequence↗

PubMed2005

The effect of a bacteriophage on diversification of the opportunistic bacterial pathogen, Pseudomonas aeruginosa.

Pseudomonas aeruginosa is an opportunistic human pathogen that colonizes the lungs of cystic fibrosis (CF) patients. CF lungs often contain a diverse range of P. aeruginosa phenotypes, some of which are likely to contribute to the persistence of infection, yet the causes of diversity are unclear. While the ecological heterogeneity of the lung environment and therapeutic regimes are probable factors, a role for parasitic bacteriophage cannot be ruled out. Parasites have been implicated as a key ecological variable driving the evolution of diversity in host populations. PP7 drove cycles of morphological diversification in host populations of P. aeruginosa due to the de novo evolution of small-rough colony variants that coexisted with large diffuse colony morph bacteria. In the absence of phage, bacteria only displayed the large diffuse colony morphology of the wild-type. Further assays revealed there to be two distinct types of resistant bacteria; these had very different ecological phenotypes, yet each carried a cost of resistance.

Colony Count, Microbial↗

PubMed1983

Evidence for gene sharing in the nitrate reduction systems of Pseudomonas aeruginosa.

Pseudomonas aeruginosa mutants unable to assimilate or dissimilate nitrate were isolated. Transduction and reversion analyses of these mutants revealed that single genetic lesions are responsible for the double phenotypes. The mutants were divided into two classes based on the ability to utilize hypoxanthine. It can be concluded from this study that at least two genes are shared between the two nitrate reduction systems.

Coenzymes↗

PubMed2006

Dynamics of development and dispersal in sessile microbial communities: examples from Pseudomonas aeruginosa and Pseudomonas putida model biofilms.

Surface-associated microbial communities in many cases display dynamic developmental patterns. Model biofilms formed by Pseudomonas aeruginosa and Pseudomonas putida in laboratory flow-chamber setups represent examples of such behaviour. Dependent on the experimental conditions the bacteria in these model biofilms develop characteristic multicellular structures through a series of distinct steps where cellular migration plays an important role. Despite the appearance of these characteristic developmental patterns in the model biofilms the available evidence suggest that the biofilm forming organisms do not possess comprehensive genetic programs for biofilm development. Instead the bacteria appear to have evolved a number of different mechanisms to optimize surface colonization, of which they express a subset in response to the prevailing environmental conditions. These mechanisms include the ability to regulate cellular adhesiveness and migration in response to micro-environmental signals including those secreted by the bacteria themselves.

Adaptation, Physiological↗

PubMed1998

Constitutive choline transport in Pseudomonas aeruginosa.

Pseudomonas aeruginosa has a choline uptake system which is expressed in bacteria grown in the presence of succinate and ammonium chloride as the carbon and nitrogen source, respectively. This system obeys Michaelis-Menten kinetics with an apparent Km value of 53 microM; its activity is not inhibited by high osmolarities in the medium but is partially inhibited by choline metabolites such as betaine and dimethylglycine.

Ammonium Chloride↗

PubMed1982

Characterization and genetic mapping of fructose phosphotransferase mutations in Pseudomonas aeruginosa.

Pseudomonas aeruginosa transports and phosphorylates fructose via a phosphoenolpyruvate-dependent fructose phosphotransferase system (PTS). Mutant strains deficient in both PTS activity and glucose-6-phosphate dehydrogenase activity were isolated and were used to select mannitol-utilizing revertant strains singly deficient in PTS activity. These mutants were unable to utilize fructose as a carbon source and failed to accumulate exogenously provided [14C]fructose, and crude cell extracts lacked phosphoenolpyruvate-dependent fructose PTS activity. Thus, the PTS was essential for the uptake and utilization of exogenously provided fructose by P. aeruginosa. Mutations at a locus designated pts, which resulted in a loss of PTS activity, exhibited 57% linkage to argF at 55 min on the chromosome in plasmid R68.45-mediated conjugational crosses. The pts mutations in four independently isolated mutant strains exhibited from 11 to 20% linkage to argF, and one of these mutations exhibited 3% linkage to lys-9015 in phage F116L-mediated transductional crosses.

Chromosome Mapping↗

PubMed2004

Single live cell imaging of chromosomes in chloramphenicol-induced filamentous Pseudomonas aeruginosa.

Pseudomonas aeruginosa is a leading opportunistic pathogen in human infections, and it is renowned for its intrinsic resistance to structurally and functionally unrelated antibiotics. Filamentation induced by antibiotics appears to trigger bacteria to depart from a normal growth phase and enter a stationary growth phase. As antibiotic concentrations decline below a therapeutic range, filamentous bacteria begin to divide normally, leading to a more rapid regrowth of the bacteria. Furthermore, filamentous bacteria are associated with an increase in endotoxin release. Moreover, the immune system of a patient needs to cope with uncharacteristic filamentous bacteria. Thus, it is biologically and clinically significant to study and understand bacterial filamentation. In this study, we investigate the frequencies, conditions, and characteristics of a filamentous P. aeruginosa at single cell and single chromosome resolutions. Our results show that filamentous cells (elongated rods) contain multiple copies of the cell's chromosome. It appears that the unsuccessful segregation of replicated chromosomes in an individual cell accompanies the formation of undivided filamentous cells. The quantity of chromosomes and the length of the filamentous wild-type cells increase as the chloramphenicol concentration increases to 50 and 250 microg/mL, suggesting that chloramphenicol induces the filamentation. Filamentation in three strains of P. aeruginosa depends on the expression level of efflux pump (MexAB-OprM) and the minimum inhibitory concentration of chloramphenicol. This study also opens up the new possibility of real-time monitoring of modes of actions of antibiotics in live cells with both temporal and spatial resolution.

Bacterial Outer Membrane Proteins↗

PubMed1976

Nosocomial infection with gentamicin-carbenicillin-resistant Pseudomonas aeruginosa.

Pseudomonas aeruginosa resistant to both gentamicin and carbenicillin was isolated with increasing frequency at the Cincinnati Veterans Administration Hospital during the period 1971 to 1974. A comparison of patients from whom P. aeruginosa was isolated during this period failed to reveal any significant clinical differences between the patients colonized or infected with resistant organisms and those colonized or infected with susceptible organisms. Overt clinical infection attributable to either organism was rare. The antibiotic-resistant organisms were isolated most frequently from urine. Isolation of the antibiotic-resistant organisms was more frequent from patients who had previously received gentamicin.

Anti-Bacterial Agents↗

PubMed2004

Biofilm formation by the small colony variant phenotype of Pseudomonas aeruginosa.

Pseudomonas aeruginosa is an ubiquitous environmental bacterium and an opportunistic human pathogen. Not only in most natural habitats but also within the human host, e.g. within the chronically infected cystic fibrosis lung, P. aeruginosa is associated with surfaces in structures known as biofilms. These functional communities represent a unique mode of bacterial growth where bacteria display particular phenotypes that are fundamentally different from planktonic cells. In this review the issue of the molecular mechanisms underlying the emergence of small colony variant (SCV) P. aeruginosa morphotypes that are especially capable of forming biofilms is addressed. It is assumed that the expression of the chaperone usher pathway (cup) genes encoding putative fimbrial adhesins is responsible for the phenotypic switch to an autoaggregative SCV phenotype. The elucidation of phenotypic switching in response to environmental stimuli will significantly increase our understanding of regulatory processes during bacterial adaptation and might be the basis for the initiation of the development of new antimicrobial treatment strategies.

Adhesins, Bacterial↗

PubMed2002

Molecular epidemiology of Pseudomonas aeruginosa.

Pseudomonas aeruginosa is a serious opportunistic pathogen in certain compromised hosts, such as those with cystic fibrosis, thermal burns and cancer. It also causes less severe noninvasive disease, such as otitis externa and hot tub folliculitis, in normal hosts. P. aeruginosa is phenotypically very unstable, particularly in patients with chronic infection. Phenotypic typing techniques are useful for understanding the epidemiology of acute infections, but they are limited by their discriminatory power and by their inability to group isolates that are phenotypically unrelated but genetically homologous. Molecular typing techniques, developed over the past decade, are highly discriminatory and are useful for typing strains from patients with chronic infection where the bacterial phenotype is unstable; this is particularly true in cystic fibrosis, where patients often are infected with the same strain for several decades, but the bacteria undergo phenotypic alteration. Molecular typing techniques, which have proven useful in typing P. aeruginosa for epidemiological purposes, include pulsed field gel electrophoresis, restriction fragment length polymorphic DNA analysis, random amplified polymorphic DNA analysis, repetitive extrapalindromic PCR analysis, and multilocus sequence typing. These methods are generally only available in specialized laboratories, but they should be used when data from phenotypic typing analysis are ambiguous or when phenotypic methods are unreliable, such as in cystic fibrosis.

Bacterial Typing Techniques↗

PubMed1983

In vitro response of human T cells to Pseudomonas aeruginosa.

Pseudomonas aeruginosa is a gram-negative bacillus that is a major cause of morbidity and mortality in immunosuppressed patients, burn patients, and patients with cystic fibrosis. Although immunity to these bacteria has been associated with serum antibody, more recent evidence suggests that T-cell-mediated immunity may also be important. To evaluate human T-cell responsiveness to these bacteria, the optimal conditions were determined for in vitro proliferation of human peripheral blood lymphocytes and T-lymphocytes to Fisher-Devlin immunotype 1 P. aeruginosa. The proliferative response of normal adult peripheral blood lymphocytes to heat-killed P. aeruginosa was studied in 34 subjects (range, 7,600 to 111,500 net cpm). Analysis of cell subpopulations indicated that T-lymphocytes are the major proliferating cells and that this response is enhanced by the presence of adherent cells. Data from fetal cord lymphocyte responses suggest that the proliferation seen in normal adult lymphocytes is induced by antigenic and not mitogenic stimulation.

Age Factors↗

PubMed2005

Rhamnolipids modulate swarming motility patterns of Pseudomonas aeruginosa.

Pseudomonas aeruginosa is capable of twitching, swimming, and swarming motility. The latter form of translocation occurs on semisolid surfaces, requires functional flagella and biosurfactant production, and results in complex motility patterns. From the point of inoculation, bacteria migrate as defined groups, referred to as tendrils, moving in a coordinated manner capable of sensing and responding to other groups of cells. We were able to show that P. aeruginosa produces extracellular factors capable of modulating tendril movement, and genetic analysis revealed that modulation of these movements was dependent on rhamnolipid biosynthesis. An rhlB mutant (deficient in mono- and dirhamnolipid production) and an rhlC mutant (deficient in dirhamnolipid production) exhibited altered swarming patterns characterized by irregularly shaped tendrils. In addition, agar supplemented with rhamnolipid-containing spent supernatant inhibited wild-type (WT) swarming, whereas agar supplemented with spent supernatant from mutants that do not make rhamnolipids had no effect on WT P. aeruginosa swarming. Addition of purified rhamnolipids to swarming medium also inhibited swarming motility of the WT strain. We also show that a sadB mutant does not sense and/or respond to other groups of swarming cells and this mutant was capable of swarming on media supplemented with rhamnolipid-containing spent supernatant or purified rhamnolipids. The abilities to produce and respond to rhamnolipids in the context of group behavior are discussed.

Bacterial Proteins↗

PubMed2006

Biosynthesis of gold nanoparticles using Pseudomonas aeruginosa.

Pseudomonas aeruginosa were used for extra-cellular biosynthesis of gold nanoparticles (Au NPs). Consequently, Au NPs were formed due to reduction of gold ion by bacterial cell supernatant of P. aeruginosa ATCC 90271, P. aeruginosa (2) and P. aeruginosa (1). The UV-vis and fluorescence spectra of the bacterial as well as chemical prepared Au NPs were recorded. Transmission electron microscopy (TEM) micrograph showed the formation of well-dispersed gold nanoparticles in the range of 15-30 nm. The process of reduction being extra-cellular and may lead to the development of an easy bioprocess for synthesis of Au NPs.

Extracellular Space↗

PubMed2003

Conservation of genome content and virulence determinants among clinical and environmental isolates of Pseudomonas aeruginosa.

Pseudomonas aeruginosa is a ubiquitous environmental bacterium capable of causing a variety of life-threatening human infections. The genetic basis for preferential infection of certain immunocompromised patients or individuals with cystic fibrosis by P. aeruginosa is not understood. To establish whether variation in the genomic repertoire of P. aeruginosa strains can be associated with a particular type of infection, we used a whole-genome DNA microarray to determine the genome content of 18 strains isolated from the most common human infections and environmental sources. A remarkable conservation of genes including those encoding nearly all known virulence factors was observed. Phylogenetic analysis of strain-specific genes revealed no correlation between genome content and infection type. Clusters of strain-specific genes in the P. aeruginosa genome, termed variable segments, appear to be preferential sites for the integration of novel genetic material. A specialized cloning vector was developed for capture and analysis of these genomic segments. With this capture system a site associated with the strain-specific ExoU cytotoxin-encoding gene was interrogated and an 80-kb genomic island carrying exoU was identified. These studies demonstrate that P. aeruginosa strains possess a highly conserved genome that encodes genes important for survival in numerous environments and allows it to cause a variety of human infections. The acquisition of novel genetic material, such as the exoU genomic island, through horizontal gene transfer may enhance colonization and survival in different host environments.

Bacterial Proteins↗

PubMed1992

Phosphate taxis in Pseudomonas aeruginosa.

Pseudomonas aeruginosa was shown to be attracted to phosphate. The chemotactic response was induced by phosphate starvation. The specificity of chemoreceptors for phosphate was high so that no other tested phosphorus compounds elicited a chemotactic response as strong as that elicited by phosphate. Competition experiments showed that the chemoreceptors for phosphate appeared to be different from those for the common amino acids. Mutants constitutive for alkaline phosphatase showed the chemotactic response to phosphate regardless of whether the cells were starved for phosphate.

Alkaline Phosphatase↗

PubMed2004

The transcriptional regulator AlgR controls cyanide production in Pseudomonas aeruginosa.

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 approximately 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 micromol of HCN/mg of protein versus 2.4 +/- 0.40 micromol 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.

Bacterial Proteins↗