Fitness of isogenic colony morphology variants of Pseudomonas aeruginosa in murine airway infection.

2.50
Hdl Handle:
http://hdl.handle.net/10033/35972
Title:
Fitness of isogenic colony morphology variants of Pseudomonas aeruginosa in murine airway infection.
Authors:
Rakhimova, Elza; Munder, Antje; Wiehlmann, Lutz; Bredenbruch, Florian; Tümmler, Burkhard
Abstract:
Chronic lung infections with Pseudomonas aeruginosa are associated with the diversification of the persisting clone into niche specialists and morphotypes, a phenomenon called 'dissociative behaviour'. To explore the potential of P. aeruginosa to change its morphotype by single step loss-of-function mutagenesis, a signature-tagged mini-Tn5 plasposon library of the cystic fibrosis airway isolate TBCF10839 was screened for colony morphology variants under nine different conditions in vitro. Transposon insertion into 1% of the genome changed colony morphology into eight discernable morphotypes. Half of the 55 targets encode features of primary or secondary metabolism whereby quinolone production was frequently affected. In the other half the transposon had inserted into genes of the functional categories transport, regulation or motility/chemotaxis. To mimic dissociative behaviour of isogenic strains in lungs, pools of 25 colony morphology variants were tested for competitive fitness in an acute murine airway infection model. Six of the 55 mutants either grew better or worse in vivo than in vitro, respectively. Metabolic proficiency of the colony morphology variant was a key determinant for survival in murine airways. The most common morphotype of self-destructive autolysis did unexpectedly not impair fitness. Transposon insertions into homologous genes of strain PAO1 did not reproduce the TBCF10839 mutant morphotypes for 16 of 19 examined loci pointing to an important role of the genetic background on colony morphology. Depending on the chosen P. aeruginosa strain, functional genome scans will explore other areas of the evolutionary landscape. Based on our discordant findings of mutant phenotypes in P. aeruginosa strains PAO1, PA14 and TBCF10839, we conclude that the current focus on few reference strains may miss modes of niche adaptation and dissociative behaviour that are relevant for the microevolution of complex traits in the wild.
Affiliation:
Clinical Research Group, OE6710, Hanover Medical School, Hanover, Germany.
Citation:
Fitness of isogenic colony morphology variants of Pseudomonas aeruginosa in murine airway infection. 2008, 3 (2):e1685 PLoS ONE
Journal:
PLoS ONE
Issue Date:
2008
URI:
http://hdl.handle.net/10033/35972
DOI:
10.1371/journal.pone.0001685
PubMed ID:
18301762
Additional Links:
http://www.plosone.org/article/info:doi/10.1371/journal.pone.0001685
Type:
Article
Language:
en
ISSN:
1932-6203
Appears in Collections:
Publications of Dept. Cell Biology (ZB)

Full metadata record

DC FieldValue Language
dc.contributor.authorRakhimova, Elza-
dc.contributor.authorMunder, Antje-
dc.contributor.authorWiehlmann, Lutz-
dc.contributor.authorBredenbruch, Florian-
dc.contributor.authorTümmler, Burkhard-
dc.date.accessioned2008-08-20T12:52:47Z-
dc.date.available2008-08-20T12:52:47Z-
dc.date.issued2008-
dc.identifier.citationFitness of isogenic colony morphology variants of Pseudomonas aeruginosa in murine airway infection. 2008, 3 (2):e1685 PLoS ONEen
dc.identifier.issn1932-6203-
dc.identifier.pmid18301762-
dc.identifier.doi10.1371/journal.pone.0001685-
dc.identifier.urihttp://hdl.handle.net/10033/35972-
dc.description.abstractChronic lung infections with Pseudomonas aeruginosa are associated with the diversification of the persisting clone into niche specialists and morphotypes, a phenomenon called 'dissociative behaviour'. To explore the potential of P. aeruginosa to change its morphotype by single step loss-of-function mutagenesis, a signature-tagged mini-Tn5 plasposon library of the cystic fibrosis airway isolate TBCF10839 was screened for colony morphology variants under nine different conditions in vitro. Transposon insertion into 1% of the genome changed colony morphology into eight discernable morphotypes. Half of the 55 targets encode features of primary or secondary metabolism whereby quinolone production was frequently affected. In the other half the transposon had inserted into genes of the functional categories transport, regulation or motility/chemotaxis. To mimic dissociative behaviour of isogenic strains in lungs, pools of 25 colony morphology variants were tested for competitive fitness in an acute murine airway infection model. Six of the 55 mutants either grew better or worse in vivo than in vitro, respectively. Metabolic proficiency of the colony morphology variant was a key determinant for survival in murine airways. The most common morphotype of self-destructive autolysis did unexpectedly not impair fitness. Transposon insertions into homologous genes of strain PAO1 did not reproduce the TBCF10839 mutant morphotypes for 16 of 19 examined loci pointing to an important role of the genetic background on colony morphology. Depending on the chosen P. aeruginosa strain, functional genome scans will explore other areas of the evolutionary landscape. Based on our discordant findings of mutant phenotypes in P. aeruginosa strains PAO1, PA14 and TBCF10839, we conclude that the current focus on few reference strains may miss modes of niche adaptation and dissociative behaviour that are relevant for the microevolution of complex traits in the wild.en
dc.language.isoenen
dc.relation.urlhttp://www.plosone.org/article/info:doi/10.1371/journal.pone.0001685en
dc.subject.meshAnimalsen
dc.subject.meshCystic Fibrosisen
dc.subject.meshDNA Transposable Elementsen
dc.subject.meshMiceen
dc.subject.meshMutagenesisen
dc.subject.meshPhenotypeen
dc.subject.meshPseudomonas Infectionsen
dc.subject.meshPseudomonas aeruginosaen
dc.subject.meshRespiratory Tract Infectionsen
dc.subject.meshSelection (Genetics)en
dc.subject.meshVirulenceen
dc.titleFitness of isogenic colony morphology variants of Pseudomonas aeruginosa in murine airway infection.en
dc.typeArticleen
dc.contributor.departmentClinical Research Group, OE6710, Hanover Medical School, Hanover, Germany.en
dc.identifier.journalPLoS ONEen

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