| |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||

Infectious Diseases Research Group, Department of Microbiology and Immunology,1 Department of Medicine,2 Siebens-Drake Medical Research Institute, University of Western Ontario, London, Ontario, Canada; Department of Microbiology, University of Manitoba, Winnipeg, Canada,3 School of Chemistry and EastChem, College of Science and Engineering,4 Centre for Infectious Diseases, University of Edinburgh, Edinburgh, Scotland5
Received 30 January 2007/ Accepted 20 February 2007
Using a conditional mutagenesis strategy we demonstrate here that a gene cluster encoding putative aminoarabinose (Ara4N) biosynthesis enzymes is essential for the viability of Burkholderia cenocepacia. Loss of viability is associated with dramatic changes in bacterial cell morphology and ultrastructure, increased permeability to propidium iodide, and sensitivity to sodium dodecyl sulfate, suggesting a general cell envelope defect caused by the lack of Ara4N.
Published ahead of print on 2 March 2007.
This article has been cited by other articles:
| Appl. Environ. Microbiol. | Infect. Immun. | Eukaryot. Cell |
|---|---|---|
| Mol. Cell. Biol. | J. Virol. | Microbiol. Mol. Biol. Rev. |
| ALL ASM JOURNALS |