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Journal of Bacteriology, August 2006, p. 5428-5438, Vol. 188, No. 15
0021-9193/06/$08.00+0     doi:10.1128/JB.01956-05
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

Role of Histone-Like Proteins H-NS and StpA in Expression of Virulence Determinants of Uropathogenic Escherichia coli

Claudia M. Müller,1 Ulrich Dobrindt,1 Gábor Nagy,2 Levente Emödy,2 Bernt Eric Uhlin,3 and Jörg Hacker1*

Institut für Molekulare Infektionsbiologie, Universität Würzburg, D-97070 Würzburg, Germany,1 Institute of Medical Microbiology and Immunology, University of Pécs Medical School, H-7624 Pécs, Hungary,2 Department of Molecular Biology, Umeå University, S-90187 Umeå, Sweden3

Received 21 December 2005/ Accepted 12 May 2006

The histone-like protein H-NS is a global regulator in Escherichia coli that has been intensively studied in nonpathogenic strains. However, no comprehensive study on the role of H-NS and its paralogue, StpA, in gene expression in pathogenic E. coli has been carried out so far. Here, we monitored the global effects of H-NS and StpA in a uropathogenic E. coli isolate by using DNA arrays. Expression profiling revealed that more than 500 genes were affected by an hns mutation, whereas no effect of StpA alone was observed. An hns stpA double mutant showed a distinct gene expression pattern that differed in large part from that of the hns single mutant. This suggests a direct interaction between the two paralogues and the existence of distinct regulons of H-NS and an H-NS/StpA heteromeric complex. hns mutation resulted in increased expression of alpha-hemolysin, fimbriae, and iron uptake systems as well as genes involved in stress adaptation. Furthermore, several other putative virulence genes were found to be part of the H-NS regulon. Although the lack of H-NS, either alone or in combination with StpA, has a huge impact on gene expression in pathogenic E. coli strains, its effect on virulence is ambiguous. At a high infection dose, hns mutants trigger more sudden lethality due to their increased acute toxicity in murine urinary tract infection and sepsis models. At a lower infectious dose, however, mutants lacking H-NS are attenuated through their impaired growth rate, which can only partially be compensated for by the higher expression of numerous virulence factors.

* Corresponding author. Mailing address: Institut für Molekulare Infektionsbiologie, Röntgenring 11, D-97070 Würzburg, Germany. Phone: 49 (0)931 312575. Fax: 49 (0)931 312578. E-mail: j.hacker{at}mail.uni-wuerzburg.de.

Journal of Bacteriology, August 2006, p. 5428-5438, Vol. 188, No. 15
0021-9193/06/$08.00+0     doi:10.1128/JB.01956-05
Copyright © 2006, American Society for Microbiology. All Rights Reserved.



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