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Lee, Daniel G.; Urbach, Jonathan M.; Wu, Gang; Liberati, Nicole T.; Feinbaum, Rhonda; Miyata, Sachiko; Diggins, Lenard T.; He, Jianxin; Saucier, Maude; Déziel, Éric; Friedman, Lisa; Li, Li; Grills, George S.; Montgomery, Kate; Kucherlapati, Raju; Rahme, Laurence G.; Ausubel, Frederick M.

doi:10.1186/gb-2006-7-10-r90

Cited by 481 publications

(317 citation statements)

References 40 publications

(64 reference statements)

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“…Please note that the ter locus is located in PAO1 sublines PAO1-DSM and MPAO1 opposite the origin of replication (Fig. 1B) as has been observed in all other sequenced P. aeruginosa chromosomes (21,25,39). Hence, the first sequenced PAO1-UW strain with its asymmetric localization of the terminus of replication has to be considered an exception to the global genome architecture of P. aeruginosa.…”

Section: Resultsmentioning

confidence: 99%

“…Moreover, progeny of the strain PAO1 that had been identical in its physical map with the original strain stored in Bruce Holloway's laboratory (12) turned out to harbor numerous deviations from the published PAO1 sequence. The major differences of sublines MPAO1 and PAO1-DSM from the genomic sequence of the strain PAO1-UW (36) are a synteny of genes identical to that of all other sequenced P. aeruginosa strains (21,25,39), a duplication of an RGP prophage carrying a distinct integrase and putative protein serine/ threonine phosphotransferases of unknown function as well as numerous SNPs and short indels. These variations that make up 0.2% of the whole-genome sequence were found to be associated with an impact on virulence and fitness.…”

Section: Discussionmentioning

confidence: 99%

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Genome Diversity ofPseudomonas aeruginosaPAO1 Laboratory Strains

et al. 2010

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Pseudomonas aeruginosa PAO1 is the most commonly used strain for research on this ubiquitous and metabolically versatile opportunistic pathogen. Strain PAO1, a derivative of the original Australian PAO isolate, has been distributed worldwide to laboratories and strain collections. Over decades discordant phenotypes of PAO1 sublines have emerged. Taking the existing PAO1-UW genome sequence (named after the University of Washington, which led the sequencing project) as a blueprint, the genome sequences of reference strains MPAO1 and PAO1-DSM (stored at the German Collection for Microorganisms and Cell Cultures [DSMZ]) were resolved by physical mapping and deep short read sequencing-by-synthesis. MPAO1 has been the source of near-saturation libraries of transposon insertion mutants, and PAO1-DSM is identical in its SpeI-DpnI restriction map with the original isolate. The major genomic differences of MPAO1 and PAO1-DSM in comparison to PAO1-UW are the lack of a large inversion, a duplication of a mobile 12-kb prophage region carrying a distinct integrase and protein phosphatases or kinases, deletions of 3 to 1,006 bp in size, and at least 39 single-nucleotide substitutions, 17 of which affect protein sequences. The PAO1 sublines differed in their ability to cope with nutrient limitation and their virulence in an acute murine airway infection model. Subline PAO1-DSM outnumbered the two other sublines in late stationary growth phase. In conclusion, P. aeruginosa PAO1 shows an ongoing microevolution of genotype and phenotype that jeopardizes the reproducibility of research. High-throughput genome resequencing will resolve more cases and could become a proper quality control for strain collections.The metabolically versatile Pseudomonas aeruginosa is an opportunistic pathogen of plants, animals, and humans and is ubiquitously distributed in soil and aquatic habitats. The common reference strain is P. aeruginosa PAO1, a spontaneous chloramphenicol-resistant mutant of the original PAO strain (earlier called "P. aeruginosa strain 1") that had been isolated in 1954 from a wound in Melbourne, Australia (9, 10). This PAO1 strain from Bruce Holloway's laboratory has become the reference strain for Pseudomonas genetics and functional analyses of the physiology and metabolism of this gammaproteobacterium. A genetic map of its chromosome was generated by exploiting the mechanisms of gene exchange in bacteria, i.e., transduction and conjugation (11). With the advent of pulsedfield gel electrophoresis (PFGE), a physical map of the PAO1 genome was constructed (32) and later merged with the genetic map information (12). By 2000 the PAO1 strain had been completely sequenced (36). Thereafter, the genome annotation has been continually updated and the database content and functionality have been expanded to facilitate accelerated discovery of P. aeruginosa drug targets and vaccine candidates (38). Two near-saturation libraries of transposon insertion mutants have been constructed in P. aeruginosa PAO1 as a global resource for the scient...

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Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Genome Diversity ofPseudomonas aeruginosaPAO1 Laboratory Strains

et al. 2010

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“…This time frame is consistent with the 6 h time point identified in our exposure assay that shows a difference between these two strains. Since PA14 is known to be more virulent than PAO1, with the presence of pathogenicity islands containing various types of novel virulence factors (Lee et al, 2006), we tested whether D2 macrophages are also deficient in killing PA14. Similar to what was seen with PAO1 ( Fig.…”

Section: Other Host Factors Besides Complement 5 Are Involved In the mentioning

confidence: 99%

Defect in early lung defence against Pseudomonas aeruginosa in DBA/2 mice is associated with acute inflammatory lung injury and reduced bactericidal activity in naïve macrophages

et al. 2007

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“…There are several reasons why P. aeruginosa has become an incredibly successful pathogen in the lungs of CF patients. First, P. aeruginosa is equipped with an assortment of both cell-associated and extracellular virulence factors (12). Second, this bacterium has the ability to alter or redirect central metabolic activities or virulence mechanisms to adapt to stressful environments or acquire nutrients (10,(13)(14)(15)(16) and is intrinsically resistant to many antimicrobials (17).…”

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Oral Streptococci and Nitrite-Mediated Interference of Pseudomonas aeruginosa

Scoffield

2015

Infect Immun

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The oral cavity harbors a diverse community of microbes that are physiologically unique. Oral microbes that exist in this polymicrobial environment can be pathogenic or beneficial to the host. Numerous oral microbes contribute to the formation of dental caries and periodontitis; however, there is little understanding of the role these microbes play in systemic infections. There is mounting evidence that suggests that oral commensal streptococci are cocolonized with Pseudomonas aeruginosa during cystic fibrosis pulmonary infections and that the presence of these oral streptococci contributes to improved lung function. The goal of this study was to examine the underlying mechanism by which Streptococcus parasanguinis antagonizes pathogenic P. aeruginosa. In this study, we discovered that oral commensal streptococci, including Streptococcus parasanguinis, Streptococcus sanguinis, and Streptococcus gordonii, inhibit the growth of P. aeruginosa and that this inhibition is mediated by the presence of nitrite and the production of hydrogen peroxide (H 2 O 2 ) by oral streptococci. The requirement of both H 2 O 2 and nitrite for the inhibition of P. aeruginosa is due to the generation of reactive nitrogenous intermediates (RNI), including peroxynitrite. Transposon mutagenesis showed that a P. aeruginosa mutant defective in a putative ABC transporter permease is resistant to both streptococcus/nitrite-and peroxynitrite-mediated killing. Furthermore, S. parasanguinis protects Drosophila melanogaster from killing by P. aeruginosa in a nitrite-dependent manner. Our findings suggest that the combination of nitrite and H 2 O 2 may represent a unique anti-infection strategy by oral streptococci during polymicrobial infections.T he human oral cavity provides residence to more than 700 diverse bacterial species (1). A fraction of the microbial communities that colonize the oral cavity are responsible for localized pathogenic infections, such as dental caries and aggressive periodontitis (1, 2). In contrast, other oral microbes are classified as commensal bacteria (Streptococcus parasanguinis, Streptococcus sanguinis, Streptococcus gordonii, and Streptococcus salivarius) and are involved in facilitating the attachment of pathogenic bacteria to the tooth surface (3) and modulating bacterial dysbiosis (4). Microorganisms unique to the oral cavity have been considered to be mainly involved in localized oral infections; however, there is increasing evidence that suggests that oral microbes may play a more prominent role in systemic infections (5). Oral pathogens and commensals have the ability to disseminate through the bloodstream and cause infective endocarditis (6). Moreover, periodontal pathogens have been associated with cases of atherosclerosis and respiratory tract infections (5, 7).Current evidence suggests that some oral streptococci reside in locations of the body that are distant to the oral cavity, including the respiratory tracts of cystic fibrosis (CF) patients (8). Historically, Pseudomonas aeruginosa was considered to...

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Untitled

Cited by 481 publications

References 40 publications

Genome Diversity ofPseudomonas aeruginosaPAO1 Laboratory Strains

Genome Diversity ofPseudomonas aeruginosaPAO1 Laboratory Strains

Defect in early lung defence against Pseudomonas aeruginosa in DBA/2 mice is associated with acute inflammatory lung injury and reduced bactericidal activity in naïve macrophages

Oral Streptococci and Nitrite-Mediated Interference of Pseudomonas aeruginosa

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