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Journal of Bacteriology, July 2003, p. 3718-3725, Vol. 185, No. 13
0021-9193/03/$08.00+0     DOI: 10.1128/JB.185.13.3718-3725.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.

Repression of Phenazine Antibiotic Production in Pseudomonas aureofaciens Strain 30-84 by RpeA

Cheryl A. Whistler{dagger} and Leland S. Pierson III*

Department of Plant Pathology, The University of Arizona, Tucson, Arizona 85721

Received 15 January 2003/ Accepted 9 April 2003

Pseudomonas aureofaciens strain 30-84 is a biological control bacterium that utilizes a two-component GacS/GacA regulatory system interconnected with the PhzR/PhzI quorum sensing system to positively regulate biosynthesis of phenazine antibiotics that contribute to its association with plant hosts. To date, no negative regulators of phenazine production have been identified, nor has the role of repression been studied. Here we describe a novel repressor of secondary metabolism in P. aureofaciens strain 30-84, RpeA, whose deduced amino acid sequence is similar to those of a group of putative two-component regulatory systems of unknown function found in several animal and plant-pathogenic bacteria. In minimal medium where phenazine production is very low, inactivation of the rpeA gene enhanced phenazine biosynthetic gene expression and increased phenazine production but did not increase quorum sensing signal accumulation. Furthermore, RpeA functioned to block phenazine biosynthetic gene transcription in minimal medium even when quorum-sensing signals were at a level that was sufficient for induction of phenazine gene expression in rich medium. Additionally, in the absence of rpeA, the quorum sensor PhzR was not required for phenazine production. Although repression plays a critical role in phenazine regulation, the rpeA mutation could not bypass the requirement for a functional GacS/GacA system, demonstrating that activation is required even in the absence of the RpeA repressor. This study reinforces that multiple signals, including nutrition and population density, are integrated to control the appropriate expression of phenazine antibiotics.

* Corresponding author. Mailing address: Department of Plant Pathology, P.O. Box 210036, Forbes Building, Room 204, The University of Arizona, Tucson, AZ 85721. Phone: (520) 621-9419. Fax: (520) 621-9290. E-mail: lsp{at}u.arizona.edu.

{dagger} Present address: Pacific Biomedical Research Center, Kewalo Marine Laboratory, University of Hawaii, Honolulu, HI 96813.

Journal of Bacteriology, July 2003, p. 3718-3725, Vol. 185, No. 13
0021-9193/03/$08.00+0     DOI: 10.1128/JB.185.13.3718-3725.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

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