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dc.contributor.authorWarren, A. E.
dc.contributor.authorBoulianne-Larsen, C. M.
dc.contributor.authorChandler, C. B.
dc.contributor.authorChlotti, K.
dc.contributor.authorKroll, E.
dc.contributor.authorMiller, S. R.
dc.contributor.authorTaddei, F.
dc.contributor.authorSermet-Gaudelus, I.
dc.contributor.authorFerroni, A.
dc.contributor.authorMcInnerney, Kathleen
dc.contributor.authorFranklin, Michael J.
dc.contributor.authorRosenzweig, F.
dc.date.accessioned2017-02-07T18:51:33Z
dc.date.available2017-02-07T18:51:33Z
dc.date.issued2011-09
dc.identifier.citationWarren AE, Boulianne-Larsen CM, Chandler CB, Chiotti K, Kroll E, Miller SR, Taddei F, Sermet-Gaudelus I, Ferroni A, McInnerney K, Franklin MJ, Rosenzweig F, "Genotypic and phenotypic variation in Pseudomonas aeruginosa reveals signatures of secondary infection and mutator activity in certain Cystic Fibrosis patients with chronic lung infections," Infection and Immunity 2011 79(12):4802-18en_US
dc.identifier.issn0019-9567
dc.identifier.urihttps://scholarworks.montana.edu/xmlui/handle/1/12583
dc.description.abstractEvolutionary adaptation of Pseudomonas aeruginosa to the cystic fibrosis lung is limited by genetic variation, which depends on rates of horizontal gene transfer and mutation supply. Because each may increase following secondary infection or mutator emergence, we sought to ascertain the incidence of secondary infection and genetic variability in populations containing or lacking mutators. Forty-nine strains collected over 3 years from 16 patients were phenotyped for antibiotic resistance and mutator status and were genotyped by repetitive-sequence PCR (rep-PCR), pulsed-field gel electrophoresis (PFGE), and multilocus sequence typing (MLST). Though phenotypic and genetic polymorphisms were widespread and clustered more strongly within than between longitudinal series, their distribution revealed instances of secondary infection. Sequence data, however, indicated that interlineage recombination predated initial strain isolation. Mutator series were more likely to be multiply antibiotic resistant, but not necessarily more variable in their nucleotide sequences, than nonmutators. One mutator and one nonmutator series were sequenced at mismatch repair loci and analyzed for gene content using DNA microarrays. Both were wild type with respect to mutL, but mutators carried an 8-bp mutS deletion causing a frameshift mutation. Both series lacked 126 genes encoding pilins, siderophores, and virulence factors whose inactivation has been linked to adaptation during chronic infection. Mutators exhibited loss of severalfold more genes having functions related to mobile elements, motility, and attachment. A 105-kb, 86-gene deletion was observed in one nonmutator that resulted in loss of virulence factors related to pyoverdine synthesis and elements of the multidrug efflux regulon. Diminished DNA repair activity may facilitate but not be absolutely required for rapid evolutionary change.en_US
dc.titleGenotypic and phenotypic variation in Pseudomonas aeruginosa reveals signatures of secondary infection and mutator activity in certain Cystic Fibrosis patients with chronic lung infectionsen_US
dc.typeArticleen_US
mus.citation.extentfirstpage4802en_US
mus.citation.extentlastpage4818en_US
mus.citation.issue12en_US
mus.citation.journaltitleInfection and Immunityen_US
mus.citation.volume79en_US
mus.identifier.categoryChemical & Material Sciencesen_US
mus.identifier.categoryEngineering & Computer Scienceen_US
mus.identifier.categoryHealth & Medical Sciencesen_US
mus.identifier.categoryLife Sciences & Earth Sciencesen_US
mus.identifier.doi10.1128/iai.05282-11en_US
mus.relation.collegeCollege of Engineeringen_US
mus.relation.collegeCollege of Letters & Scienceen_US
mus.relation.departmentCenter for Biofilm Engineering.en_US
mus.relation.departmentMicrobiology & Immunology.en_US
mus.relation.universityMontana State University - Bozemanen_US
mus.relation.researchgroupCenter for Biofilm Engineering.en_US
mus.data.thumbpage6en_US


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