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Genome mosaicism is conserved but not unique in Pseudomonas aeruginosa isolates from the airways of young children with cystic fibrosis
Authors:Ernst Robert K  D'Argenio David A  Ichikawa Jeffrey K  Bangera M Gita  Selgrade Sara  Burns Jane L  Hiatt Peter  McCoy Karen  Brittnacher Mitchell  Kas Arnold  Spencer David H  Olson Maynard V  Ramsey Bonnie W  Lory Stephen  Miller Samuel I
Institution:Department of Microbiology, University of Washington, Health Sciences Building, K-140, Box 357710, Seattle, WA 98195, USA.; Department of Microbiology and Molecular Genetics, Harvard Medical School, Boston, MA, 02115, USA.; Department of Pediatrics, University of Washington, Seattle, WA 98195, USA.; Department of Pediatrics, Baylor College of Medicine, Houston, TX, 77030, USA.; Division of Pulmonary Medicine, Columbus Children's Hospital, Columbus, OH, 43205, USA.; Department of Genome Sciences, University of Washington, Seattle, WA 98195, USA.; Department of Medicine, University of Washington, Seattle, WA 98195, USA.
Abstract:Pseudomonas aeruginosa strains from the chronic lung infections of cystic fibrosis (CF) patients are phenotypically and genotypically diverse. Using strain PAO1 whole genome DNA microarrays, we assessed the genomic variation in P. aeruginosa strains isolated from young children with CF (6 months to 8 years of age) as well as from the environment. Eighty-nine to 97% of the PAO1 open reading frames were detected in 20 strains by microarray analysis, while subsets of 38 gene islands were absent or divergent. No specific pattern of genome mosaicism defined strains associated with CF. Many mosaic regions were distinguished by their low G + C content; their inclusion of phage related or pyocin genes; or by their linkage to a vgr gene or a tRNA gene. Microarray and phenotypic analysis of sequential isolates from individual patients revealed two deletions of greater than 100 kbp formed during evolution in the lung. The gene loss in these sequential isolates raises the possibility that acquisition of pyomelanin production and loss of pyoverdin uptake each may be of adaptive significance. Further characterization of P. aeruginosa diversity within the airways of individual CF patients may reveal common adaptations, perhaps mediated by gene loss, that suggest new opportunities for therapy.
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