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Journal of Bacteriology, November 2008, p. 7209-7218, Vol. 190, No. 21
0021-9193/08/$08.00+0     doi:10.1128/JB.00481-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

A Functional Phenylacetic Acid Catabolic Pathway Is Required for Full Pathogenicity of Burkholderia cenocepacia in the Caenorhabditis elegans Host Model{triangledown}

Robyn J. Law, Jason N. R. Hamlin, Aida Sivro,{ddagger} Stuart J. McCorrister, Georgina A. Cardama,§ and Silvia T. Cardona*

Department of Microbiology, University of Manitoba, Winnipeg, Manitoba, Canada

Received 8 April 2008/ Accepted 26 August 2008

Burkholderia cenocepacia is a member of the Burkholderia cepacia complex, a group of metabolically versatile bacteria that have emerged as opportunistic pathogens in cystic fibrosis and immunocompromised patients. Previously a screen of transposon mutants in a rat pulmonary infection model identified an attenuated mutant with an insertion in paaE, a gene related to the phenylacetic acid (PA) catabolic pathway. In this study, we characterized gene clusters involved in the PA degradation pathway of B. cenocepacia K56-2 in relation to its pathogenicity in the Caenorhabditis elegans model of infection. We demonstrated that targeted-insertion mutagenesis of paaA and paaE, which encode part of the putative PA-coenzyme A (CoA) ring hydroxylation system, paaZ, coding for a putative ring opening enzyme, and paaF, encoding part of the putative beta-oxidation system, severely reduces growth on PA as a sole carbon source. paaA and paaE insertional mutants were attenuated for virulence, and expression of paaE in trans restored pathogenicity of the paaE mutant to wild-type levels. Interruption of paaZ and paaF slightly increased virulence. Using gene interference by ingested double-stranded RNA, we showed that the attenuated phenotype of the paaA and paaE mutants is dependent on a functional p38 mitogen-activated protein kinase pathway in C. elegans. Taken together, our results demonstrate that B. cenocepacia possesses a functional PA degradation pathway and that the putative PA-CoA ring hydroxylation system is required for full pathogenicity in C. elegans.

* Corresponding author. Mailing address: Department of Microbiology, Buller Building, Room 418, University of Manitoba, Winnipeg, Manitoba, Canada R3T 2N2. Phone: (204) 474-8997. Fax: (204) 474-7603. E-mail: cardona{at}cc.umanitoba.ca

{triangledown} Published ahead of print on 5 September 2008.

{ddagger} Present address: Department of Medical Microbiology and Infectious Diseases, Basic Medical Sciences Building Room 507, University of Manitoba, Winnipeg, Manitoba, Canada R3E 0W3.

§ Present address: Laboratory of Molecular Oncology, Quilmes National University, Bernal, Argentina.

Journal of Bacteriology, November 2008, p. 7209-7218, Vol. 190, No. 21
0021-9193/08/$08.00+0     doi:10.1128/JB.00481-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Uehlinger, S., Schwager, S., Bernier, S. P., Riedel, K., Nguyen, D. T., Sokol, P. A., Eberl, L. (2009). Identification of Specific and Universal Virulence Factors in Burkholderia cenocepacia Strains by Using Multiple Infection Hosts. Infect. Immun. 77: 4102-4110 [Abstract] [Full Text]  


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