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Journal of Bacteriology, May 2007, p. 3425-3433, Vol. 189, No. 9
0021-9193/07/$08.00+0     doi:10.1128/JB.00209-07
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

Two Distinct Pathways Supply Anthranilate as a Precursor of the Pseudomonas Quinolone Signal{triangledown}

John M. Farrow III and Everett C. Pesci*

Department of Microbiology and Immunology, The Brody School of Medicine at East Carolina University, 600 Moye Blvd., Greenville, North Carolina 27834

Received 7 February 2007/ Accepted 23 February 2007

Pseudomonas aeruginosa is an opportunistic pathogen that causes serious infections in immunocompromised patients and those with cystic fibrosis (CF). This gram-negative bacterium uses multiple cell-to-cell signals to control numerous cellular functions and virulence. One of these signals is 2-heptyl-3-hydroxy-4-quinolone, which is referred to as the Pseudomonas quinolone signal (PQS). This signal functions as a coinducer for a transcriptional regulator (PqsR) to positively control multiple virulence genes and its own synthesis. PQS production is required for virulence in multiple models of infection, and it has been shown to be produced in the lungs of CF patients infected by P. aeruginosa. One of the precursor compounds from which PQS is synthesized is the metabolite anthranilate. This compound can be derived from the conversion of chorismate to anthranilate by an anthranilate synthase or through the degradation of tryptophan via the anthranilate branch of the kynurenine pathway. In this study, we present data which help to define the kynurenine pathway in P. aeruginosa and show that the kynurenine pathway serves as a critical source of anthranilate for PQS synthesis. We also show that the kyn pathway genes are induced during growth with tryptophan and that they are autoregulated by kynurenine. This study provides solid foundations for the understanding of how P. aeruginosa produces the anthranilate that serves as a precursor to PQS and other 4-quinolones.

* Corresponding author. Mailing address: Department of Microbiology and Immunology, East Carolina University School of Medicine, BT 132, 600 Moye Blvd., Greenville, NC 27834. Phone: (252) 744-2351. Fax: (252) 744-3535. E-mail: pescie{at}ecu.edu

{triangledown} Published ahead of print on 2 March 2007.

Journal of Bacteriology, May 2007, p. 3425-3433, Vol. 189, No. 9
0021-9193/07/$08.00+0     doi:10.1128/JB.00209-07
Copyright © 2007, American Society for Microbiology. All Rights Reserved.



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