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Journal of Bacteriology, October 2009, p. 5901-5909, Vol. 191, No. 19
0021-9193/09/$08.00+0 doi:10.1128/JB.00591-09
Copyright © 2009, American Society for Microbiology. All Rights Reserved.
Mutational Analysis of Burkholderia thailandensis Quorum Sensing and Self-Aggregation 
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Josephine R. Chandler,1
Breck A. Duerkop,1,
Aaron Hinz,2
T. Eoin West,3
Jake P. Herman,4
Mair E. A. Churchill,4
Shawn J. Skerrett,3 and
E. Peter Greenberg1*
Department of Microbiology, University of Washington School of Medicine, Campus Box 357242, 1959 N.E. Pacific St., Seattle, Washington 98195,1 Department of Genome Sciences, University of Washington School of Medicine, Campus Box 355065, 1705 N.E. Pacific St., Seattle, Washington 98195,2 Department of Medicine, University of Washington School of Medicine, Harborview Medical Center, Campus Box 359640, 325 9th Avenue, Seattle, Washington 98104,3 Department of Pharmacology, Program in Biomolecular Structure, Campus Box 8303, University of Colorado—Denver School of Medicine, Aurora, Colorado 800454
Received 6 May 2009/ Accepted 20 July 2009
Acyl-homoserine lactone (acyl-HSL) quorum-sensing signaling is common to many Proteobacteria. Acyl-HSLs are synthesized by the LuxI family of synthases, and the signal response is mediated by members of the LuxR family of transcriptional regulators. Burkholderia thailandensis is a member of a closely related cluster of three species, including the animal pathogens Burkholderia mallei and Burkholderia pseudomallei. Members of this group have similar luxI and luxR homologs, and these genes contribute to B. pseudomallei and B. mallei virulence. B. thailandensis possesses three pairs of luxI-luxR homologs. One of these pairs, BtaI2-BtaR2, has been shown to produce and respond to 3OHC10-HSL and to control the synthesis of an antibiotic. By using a markerless-exhange method, we constructed an assortment of B. thailandensis quorum-sensing mutants, and we used these mutants to show that BtaI1 is responsible for C8-HSL production and BtaI3 is responsible for 3OHC8-HSL production. We also show that a strain incapable of acyl-HSL production is capable of growth on the same assortment of carbon and nitrogen sources as the wild type. Furthermore, this mutant shows no loss of virulence compared to the wild type in mice. However, the wild type self-aggregates in minimal medium, whereas the quorum-sensing mutant does not. The wild-type aggregation phenotype is recovered by addition of the BtaI1-R1 HSL signal C8-HSL. We propose that the key function of the BtaR1-BtaI1 quorum-sensing system is to cause cells to gather into aggregates once a sufficient population has been established.
* Corresponding author. Mailing address: Department of Microbiology, University of Washington School of Medicine, 1705 N.E. Pacific Street, Campus Box 357242, Seattle, WA 98195-7242. Phone: (206) 616-2881. Fax: (206) 616-2968. E-mail: epgreen{at}u.washington.edu
Published ahead of print on 31 July 2009.
Supplemental material for this article may be found at http://jb.asm.org/.
Present address: Howard Hughes Medical Institute and the Department of Immunology, University of Texas Southwestern Medical Center, Dallas, TX 75390.
Journal of Bacteriology, October 2009, p. 5901-5909, Vol. 191, No. 19
0021-9193/09/$08.00+0 doi:10.1128/JB.00591-09
Copyright © 2009, American Society for Microbiology. All Rights Reserved.
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