Journal of Bacteriology, October 2007, p. 6743-6750, Vol. 189, No. 19
0021-9193/07/$08.00+0 doi:10.1128/JB.00889-07
Copyright © 2007, American Society for Microbiology. All Rights Reserved.
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Faculty of Life Sciences, University of Manchester, Oxford Road, Manchester M13 9PT, United Kingdom,1 Génétique Moléculaire, Génomique, Microbiologie, UMR 7156 Université Louis Pasteur—CNRS, F-67083 Strasbourg, France,2 Faculty of Medicine, University of Liverpool, Liverpool L69 3GA, United Kingdom3
Received 7 June 2007/ Accepted 25 July 2007
Pseudomonas aeruginosa is an opportunistic pathogen that causes a number of infections in humans, but is best known for its association with cystic fibrosis. It is able to use a wide range of sulfur compounds as sources of sulfur for growth. Gene expression in response to changes in sulfur supply was studied in P. aeruginosa E601, a cystic fibrosis isolate that displays mucin sulfatase activity, and in P. aeruginosa PAO1. A large family of genes was found to be upregulated by sulfate limitation in both isolates, encoding sulfatases and sulfonatases, transport systems, oxidative stress proteins, and a sulfate-regulated TonB/ExbBD complex. These genes were localized in five distinct islands on the genome and encoded proteins with a significantly reduced content of cysteine and methionine. Growth of P. aeruginosa E601 with mucin as the sulfur source led not only to a sulfate starvation response but also to induction of genes involved with type III secretion systems.
Published ahead of print on 3 August 2007.
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