title: The cep quorum-sensing system of Burkholderia cepacia H111 controls biofilm formation and swarming motility.
abstract: Burkholderia cepacia and Pseudomonas aeruginosa often co-exist as mixed biofilms in the lungs of patients suffering from cystic fibrosis (CF). Here, the isolation of random mini-Tn5 insertion mutants of B. cepacia H111 defective in biofilm formation on an abiotic surface is reported. It is demonstrated that one of these mutants no longer produces N-acylhomoserine lactones (AHLs) due to an inactivation of the cepR gene. cepR and the cepI AHL synthase gene together constitute the cep quorum-sensing system of B. cepacia. By using a gene replacement method, two defined mutants, H111-I and H111-R, were constructed in which cepI and cepR, respectively, had been inactivated. These mutants were used to demonstrate that biofilm formation by B. cepacia H111 requires a functional cep quorum-sensing system. A detailed quantitative analysis of the biofilm structures formed by wild-type and mutant strains suggested that the quorum-sensing system is not involved in the regulation of initial cell attachment, but rather controls the maturation of the biofilm. Furthermore, it is shown that B. cepacia is capable of swarming motility, a form of surface translocation utilized by various bacteria to rapidly colonize appropriate substrata. Evidence is provided that swarming motility of B. cepacia is quorum-sensing-regulated, possibly through the control of biosurfactant production. Complementation of the cepR mutant H111-R with different biosurfactants restored swarming motility while biofilm formation was not significantly increased. This result suggests that swarming motility per se is not essential for biofilm formation on abiotic surfaces.
authors.affiliation: Lehrstuhl für Mikrobiologie, Technische Universität München, Am Hochanger 4, 85350 Freising, Germany1.
authors.forename: Birgit
authors.initials: B
authors.lastname: Huber
authors.affiliation: Lehrstuhl für Mikrobiologie, Technische Universität München, Am Hochanger 4, 85350 Freising, Germany1.
authors.forename: Kathrin
authors.initials: K
authors.lastname: Riedel
authors.affiliation: Department of Microbiology, DTU, Building 301, 2800 Lyngby, Denmark2.
authors.forename: Morten
authors.initials: M
authors.lastname: Hentzer
authors.affiliation: Department of Microbiology, DTU, Building 301, 2800 Lyngby, Denmark2.
authors.forename: Arne
authors.initials: A
authors.lastname: Heydorn
authors.affiliation: Lehrstuhl für Mikrobiologie, Technische Universität München, Am Hochanger 4, 85350 Freising, Germany1.
authors.forename: Astrid
authors.initials: A
authors.lastname: Gotschlich
authors.affiliation: Department of Microbiology, DTU, Building 301, 2800 Lyngby, Denmark2.
authors.forename: Michael
authors.initials: M
authors.lastname: Givskov
authors.affiliation: Department of Microbiology, DTU, Building 301, 2800 Lyngby, Denmark2.
authors.forename: Søren
authors.initials: S
authors.lastname: Molin
authors.affiliation: Lehrstuhl für Mikrobiologie, Technische Universität München, Am Hochanger 4, 85350 Freising, Germany1.
authors.forename: Leo
authors.initials: L
authors.lastname: Eberl
mesh_terms: D001422:Bacterial Adhesion / Q000235:genetics / Q000502:physiology; D001426:Bacterial Proteins / Q000235:genetics / Q000502:physiology*; D001483:Base Sequence; D018441:Biofilms / Q000254:growth & development*; D019121:Burkholderia Infections / Q000382:microbiology; D016956:Burkholderia cepacia / Q000235:genetics / Q000472:pathogenicity / Q000502:physiology*; D003550:Cystic Fibrosis / Q000382:microbiology; D004269:DNA, Bacterial / Q000235:genetics; D005798:Genes, Bacterial; D006801:Humans; D008025:Ligases; D008168:Lung / Q000382:microbiology; D009068:Movement; D016254:Mutagenesis, Insertional; D009894:Opportunistic Infections / Q000382:microbiology; D010641:Phenotype; D013499:Surface Properties
chemical_list: D001426:Bacterial Proteins; C117246:CepR protein, Burkholderia; D004269:DNA, Bacterial; D008025:Ligases; C449816:N-acylhomoserine lactone synthase