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Journal of Bacteriology, October 2009, p. 6329-6334, Vol. 191, No. 20
0021-9193/09/$08.00+0 doi:10.1128/JB.00817-09
Copyright © 2009, American Society for Microbiology. All Rights Reserved.

Section of Molecular Genetics and Microbiology, The University of Texas at Austin, Austin, Texas,1 Department of Biological Sciences, St. Edward's University, Austin, Texas,2 Department of Medical Biology, Laval University, Québec, Canada3
Received 23 June 2009/ Accepted 31 July 2009
The opportunistic pathogen Pseudomonas aeruginosa causes a variety of infections in immunocompromised individuals, including individuals with the heritable disease cystic fibrosis. Like the carbon sources metabolized by many disease-causing bacteria, the carbon sources metabolized by P. aeruginosa at the host infection site are unknown. We recently reported that L-alanine is a preferred carbon source for P. aeruginosa and that two genes potentially involved in alanine catabolism (dadA and dadX) are induced during in vivo growth in the rat peritoneum and during in vitro growth in sputum (mucus) collected from the lungs of individuals with cystic fibrosis. The goals of this study were to characterize factors required for alanine catabolism in P. aeruginosa and to assess the importance of these factors for in vivo growth. Our results reveal that dadA and dadX are arranged in an operon and are required for catabolism of L-alanine. The dad operon is inducible by L-alanine, D-alanine, and L-valine, and induction is dependent on the transcriptional regulator Lrp. Finally, we show that a mutant unable to catabolize DL-alanine displays decreased competitiveness in a rat lung model of infection.
Published ahead of print on 7 August 2009.
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