The cep quorum-sensing system of Burkholderia cepacia H111 controls biofilm formation and swarming motility.
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.
Huber
Birgit
B
Lehrstuhl für Mikrobiologie, Technische Universität München, Am Hochanger 4, 85350 Freising, Germany1.
Riedel
Kathrin
K
Lehrstuhl für Mikrobiologie, Technische Universität München, Am Hochanger 4, 85350 Freising, Germany1.
Hentzer
Morten
M
Department of Microbiology, DTU, Building 301, 2800 Lyngby, Denmark2.
Heydorn
Arne
A
Department of Microbiology, DTU, Building 301, 2800 Lyngby, Denmark2.
Gotschlich
Astrid
A
Lehrstuhl für Mikrobiologie, Technische Universität München, Am Hochanger 4, 85350 Freising, Germany1.
Givskov
Michael
M
Department of Microbiology, DTU, Building 301, 2800 Lyngby, Denmark2.
Molin
Søren
S
Department of Microbiology, DTU, Building 301, 2800 Lyngby, Denmark2.
Eberl
Leo
L
Lehrstuhl für Mikrobiologie, Technische Universität München, Am Hochanger 4, 85350 Freising, Germany1.
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
D001426:Bacterial Proteins; C117246:CepR protein, Burkholderia; D004269:DNA, Bacterial; D008025:Ligases; C449816:N-acylhomoserine lactone synthase