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Journal of Bacteriology, April 2009, p. 2447-2460, Vol. 191, No. 8
0021-9193/09/$08.00+0     doi:10.1128/JB.01746-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.

A Burkholderia cenocepacia Orphan LuxR Homolog Is Involved in Quorum-Sensing Regulation{triangledown} ,{dagger}

Rebecca J. Malott ,1,{ddagger},§ Eoin P. O'Grady,1,{ddagger} Jessica Toller,2 Silja Inhülsen,2 Leo Eberl,2 and Pamela A. Sokol1*

Department of Microbiology and Infectious Diseases, University of Calgary, Calgary, Alberta Canada,1 Department of Microbiology, Institute of Plant Biology, University of Zurich, Zurich, Switzerland2

Received 14 December 2008/ Accepted 2 February 2009

Burkholderia cenocepacia utilizes quorum sensing to control gene expression, including the expression of genes involved in virulence. In addition to CepR and CciR, a third LuxR homolog, CepR2, was found to regulate gene expression and virulence factor production. All B. cenocepacia strains examined contained this orphan LuxR homolog, which was not associated with an adjacent N-acyl-homoserine lactone synthase gene. Expression of cepR2 was negatively autoregulated and was negatively regulated by CciR in strain K56-2. Microarray analysis and quantitative reverse transcription-PCR determined that CepR2 did not influence expression of cepIR or cciIR. However, in strain K56-2, CepR2 negatively regulated expression of several known quorum-sensing-controlled genes, including genes encoding zinc metalloproteases. CepR2 exerted positive and negative regulation on genes on three chromosomes, including strong negative regulation of a gene cluster located adjacent to cepR2. In strain H111, which lacks the CciIR quorum-sensing system, CepR2 positively regulated pyochelin production by controlling transcription of one of the operons required for the biosynthesis of the siderophore in an N-acyl-homoserine lactone-independent manner. CepR2 activation of a luxI promoter was demonstrated in a heterologous Escherichia coli host, providing further evidence that CepR2 can function in the absence of signaling molecules. This study demonstrates that the orphan LuxR homolog CepR2 contributes to the quorum-sensing regulatory network in two distinct strains of B. cenocepacia.

* Corresponding author. Mailing address: Department of Microbiology and Infectious Diseases, Faculty of Medicine, University of Calgary, Calgary, Alberta, Canada T2N 4N1. Phone: (403) 220-6037. Fax: (403) 270-2772. E-mail: psokol{at}ucalgary.ca

{triangledown} Published ahead of print on 6 February 2009.

{dagger} Supplemental material for this article may be found at http://jb.asm.org/.

{ddagger} R.J.M. and E.P.O. contributed equally to this study.

§ Present address: Department of Molecular Genetics, University of Toronto, Toronto, Ontario, Canada.

Journal of Bacteriology, April 2009, p. 2447-2460, Vol. 191, No. 8
0021-9193/09/$08.00+0     doi:10.1128/JB.01746-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.





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