@article{
 title = {Newly introduced genomic prophage islands are critical determinants of in vivo competitiveness in the Liverpool Epidemic Strain of Pseudomonas aeruginosa.},
 type = {article},
 year = {2009},
 identifiers = {[object Object]},
 keywords = {Animals,Bacterial,Bacterial: genetics,Disease Outbreaks,Drug Resistance,England,England: epidemiology,Fimbriae Proteins,Fimbriae Proteins: genetics,Genes,Genome,Humans,Multigene Family,Mutagenesis,O Antigens,O Antigens: genetics,Prophages,Prophages: genetics,Prophages: isolation & purification,Prophages: pathogenicity,Pseudomonas Infections,Pseudomonas Infections: epidemiology,Pseudomonas Infections: microbiology,Pseudomonas Phages,Pseudomonas Phages: genetics,Pseudomonas Phages: isolation & purification,Pseudomonas Phages: pathogenicity,Pseudomonas aeruginosa,Pseudomonas aeruginosa: genetics,Pseudomonas aeruginosa: isolation & purification,Pseudomonas aeruginosa: pathogenicity,Pseudomonas aeruginosa: virology,Rats,Viral,Virulence,Virulence: genetics},
 pages = {12-23},
 volume = {19},
 websites = {http://www.ncbi.nlm.nih.gov/pubmed/19047519},
 month = {1},
 id = {13dac52b-4b7d-3d40-b8af-d2d133e5d9ad},
 created = {2009-07-07T19:48:28.000Z},
 file_attached = {true},
 profile_id = {a5739547-2f49-3c98-ba0b-f787220163ed},
 last_modified = {2014-09-08T12:24:26.000Z},
 tags = {cystic-fibrosis,genomic-islands,phage,pseudomonas,pseudomonas-aeruginosa-les},
 read = {true},
 starred = {false},
 authored = {true},
 confirmed = {true},
 hidden = {false},
 citation_key = {Winstanley2009},
 source_type = {citeulike:JOUR},
 user_context = {Journal article},
 abstract = {Pseudomonas aeruginosa isolates have a highly conserved core genome representing up to 90% of the total genomic sequence with additional variable accessory genes, many of which are found in genomic islands or islets. The identification of the Liverpool Epidemic Strain (LES) in a children's cystic fibrosis (CF) unit in 1996 and its subsequent observation in several centers in the United Kingdom challenged the previous widespread assumption that CF patients acquire only unique strains of P. aeruginosa from the environment. To learn about the forces that shaped the development of this important epidemic strain, the genome of the earliest archived LES isolate, LESB58, was sequenced. The sequence revealed the presence of many large genomic islands, including five prophage clusters, one defective (pyocin) prophage cluster, and five non-phage islands. To determine the role of these clusters, an unbiased signature tagged mutagenesis study was performed, followed by selection in the chronic rat lung infection model. Forty-seven mutants were identified by sequencing, including mutants in several genes known to be involved in Pseudomonas infection. Furthermore, genes from four prophage clusters and one genomic island were identified and in direct competition studies with the parent isolate; four were demonstrated to strongly impact on competitiveness in the chronic rat lung infection model. This strongly indicates that enhanced in vivo competitiveness is a major driver for maintenance and diversifying selection of these genomic prophage genes.},
 bibtype = {article},
 author = {Winstanley, Craig and Langille, Morgan G I and Fothergill, Joanne L L and Kukavica-Ibrulj, Irena and Paradis-Bleau, Catherine and Sanschagrin, François and Thomson, Nicholas R R and Winsor, Geoff L L and Quail, Michael A A and Lennard, Nicola and Bignell, Alexandra and Clarke, Louise and Seeger, Kathy and Saunders, David and Harris, David and Parkhill, Julian and Hancock, Robert E W E and Brinkman, Fiona S L and Levesque, Roger C C},
 journal = {Genome research},
 number = {1}
}

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The identification of the Liverpool Epidemic Strain (LES) in a children's cystic fibrosis (CF) unit in 1996 and its subsequent observation in several centers in the United Kingdom challenged the previous widespread assumption that CF patients acquire only unique strains of P. aeruginosa from the environment. To learn about the forces that shaped the development of this important epidemic strain, the genome of the earliest archived LES isolate, LESB58, was sequenced. The sequence revealed the presence of many large genomic islands, including five prophage clusters, one defective (pyocin) prophage cluster, and five non-phage islands. To determine the role of these clusters, an unbiased signature tagged mutagenesis study was performed, followed by selection in the chronic rat lung infection model. Forty-seven mutants were identified by sequencing, including mutants in several genes known to be involved in Pseudomonas infection. Furthermore, genes from four prophage clusters and one genomic island were identified and in direct competition studies with the parent isolate; four were demonstrated to strongly impact on competitiveness in the chronic rat lung infection model. This strongly indicates that enhanced in vivo competitiveness is a major driver for maintenance and diversifying selection of these genomic prophage genes.","bibtype":"article","author":"Winstanley, Craig and Langille, Morgan G I and Fothergill, Joanne L L and Kukavica-Ibrulj, Irena and Paradis-Bleau, Catherine and Sanschagrin, François and Thomson, Nicholas R R and Winsor, Geoff L L and Quail, Michael A A and Lennard, Nicola and Bignell, Alexandra and Clarke, Louise and Seeger, Kathy and Saunders, David and Harris, David and Parkhill, Julian and Hancock, Robert E W E and Brinkman, Fiona S L and Levesque, Roger C C","journal":"Genome research","number":"1","bibtex":"@article{\n title = {Newly introduced genomic prophage islands are critical determinants of in vivo competitiveness in the Liverpool Epidemic Strain of Pseudomonas aeruginosa.},\n type = {article},\n year = {2009},\n identifiers = {[object Object]},\n keywords = {Animals,Bacterial,Bacterial: genetics,Disease Outbreaks,Drug Resistance,England,England: epidemiology,Fimbriae Proteins,Fimbriae Proteins: genetics,Genes,Genome,Humans,Multigene Family,Mutagenesis,O Antigens,O Antigens: genetics,Prophages,Prophages: genetics,Prophages: isolation & purification,Prophages: pathogenicity,Pseudomonas Infections,Pseudomonas Infections: epidemiology,Pseudomonas Infections: microbiology,Pseudomonas Phages,Pseudomonas Phages: genetics,Pseudomonas Phages: isolation & purification,Pseudomonas Phages: pathogenicity,Pseudomonas aeruginosa,Pseudomonas aeruginosa: genetics,Pseudomonas aeruginosa: isolation & purification,Pseudomonas aeruginosa: pathogenicity,Pseudomonas aeruginosa: virology,Rats,Viral,Virulence,Virulence: genetics},\n pages = {12-23},\n volume = {19},\n websites = {http://www.ncbi.nlm.nih.gov/pubmed/19047519},\n month = {1},\n id = {13dac52b-4b7d-3d40-b8af-d2d133e5d9ad},\n created = {2009-07-07T19:48:28.000Z},\n file_attached = {true},\n profile_id = {a5739547-2f49-3c98-ba0b-f787220163ed},\n last_modified = {2014-09-08T12:24:26.000Z},\n tags = {cystic-fibrosis,genomic-islands,phage,pseudomonas,pseudomonas-aeruginosa-les},\n read = {true},\n starred = {false},\n authored = {true},\n confirmed = {true},\n hidden = {false},\n citation_key = {Winstanley2009},\n source_type = {citeulike:JOUR},\n user_context = {Journal article},\n abstract = {Pseudomonas aeruginosa isolates have a highly conserved core genome representing up to 90% of the total genomic sequence with additional variable accessory genes, many of which are found in genomic islands or islets. The identification of the Liverpool Epidemic Strain (LES) in a children's cystic fibrosis (CF) unit in 1996 and its subsequent observation in several centers in the United Kingdom challenged the previous widespread assumption that CF patients acquire only unique strains of P. aeruginosa from the environment. To learn about the forces that shaped the development of this important epidemic strain, the genome of the earliest archived LES isolate, LESB58, was sequenced. The sequence revealed the presence of many large genomic islands, including five prophage clusters, one defective (pyocin) prophage cluster, and five non-phage islands. To determine the role of these clusters, an unbiased signature tagged mutagenesis study was performed, followed by selection in the chronic rat lung infection model. Forty-seven mutants were identified by sequencing, including mutants in several genes known to be involved in Pseudomonas infection. 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