RT Journal
A1 Winstanley, Craig
A1 Langille, Morgan G.I.
A1 Fothergill, Joanne L.
A1 Kukavica-Ibrulj, Irena
A1 Paradis-Bleau, Catherine
A1 Sanschagrin, François
A1 Thomson, Nicholas R.
A1 Winsor, Geoff L.
A1 Quail, Michael A.
A1 Lennard, Nicola
A1 Bignell, Alexandra
A1 Clarke, Louise
A1 Seeger, Kathy
A1 Saunders, David
A1 Harris, David
A1 Parkhill, Julian
A1 Hancock, Robert E.W.
A1 Brinkman, Fiona S.L.
A1 Levesque, Roger C.
T1 Newly introduced genomic prophage islands are critical determinants of in vivo competitiveness in the Liverpool Epidemic Strain of Pseudomonas aeruginosa
JF Genome Research 
JO Genome Research 
YR 2009 
FD January 01 
VO 19 
IS 1 
SP 12 
OP 23 
DO 10.1101/gr.086082.108 
UL http://genome.cshlp.org/content/19/1/12.abstract 
AB 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.