Get access

The Burkholderia cenocepacia sensor kinase hybrid AtsR is a global regulator modulating quorum-sensing signalling

Authors

  • Daniel F. Aubert,

    1. Centre for Human Immunology, Department of Microbiology, University of Western Ontario, London, Ontario, Canada, N6A 5C1
    Search for more papers by this author
  • Eoin P. O'Grady,

    1. Department of Microbiology, Immunology, and Infectious Diseases, University of Calgary, Calgary, Alberta, Canada, T2N 4N1
    Search for more papers by this author
  • Mohamad A. Hamad,

    1. Centre for Human Immunology, Department of Microbiology, University of Western Ontario, London, Ontario, Canada, N6A 5C1
    Search for more papers by this author
  • Pamela A. Sokol,

    1. Department of Microbiology, Immunology, and Infectious Diseases, University of Calgary, Calgary, Alberta, Canada, T2N 4N1
    Search for more papers by this author
  • Miguel A. Valvano

    Corresponding author
    1. Centre for Human Immunology, Department of Microbiology, University of Western Ontario, London, Ontario, Canada, N6A 5C1
      E-mail mvalvano@uwo.ca; Tel. (+1) 519 661 3427; Fax (+1) 519 661 3499.
    Search for more papers by this author

E-mail mvalvano@uwo.ca; Tel. (+1) 519 661 3427; Fax (+1) 519 661 3499.

Summary

Burkholderia cenocepacia is commonly found in the environment and also as an important opportunistic pathogen infecting patients with cystic fibrosis. Successful infection by this bacterium requires coordinated expression of virulence factors, which is achieved through different quorum sensing (QS) regulatory systems. Biofilm formation and Type 6 secretion system (T6SS) expression in B. cenocepacia K56-2 are positively regulated by QS and negatively regulated by the sensor kinase hybrid AtsR. This study reveals that in addition to affecting biofilm and T6SS activity, the deletion of atsR in B. cenocepacia leads to overproduction of other QS-regulated virulence determinants including proteases and swarming motility. Expression of the QS genes, cepIR and cciIR, was upregulated in the ΔatsR mutant and resulted in early and increased N-acylhomoserine lactone (AHL) production, suggesting that AtsR plays a role in controlling the timing and fine-tuning of virulence gene expression by modulating QS signalling. Furthermore, a ΔatsRΔcepIΔcciI mutant could partially upregulate the same virulence determinants indicating that AtsR also modulates the expression of virulence genes by a second mechanism, independently of any AHL production. Together, our results strongly suggest that AtsR is a global virulence regulator in B. cenocepacia.

Get access to the full text of this article

Ancillary