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Infection and Immunity, February 2002, p. 1027-1031, Vol. 70, No. 2
0019-9567/01/$04.00+0     DOI: 70.2.1027-1031.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.

Urease of Enterohemorrhagic Escherichia coli: Evidence for Regulation by Fur and a trans-Acting Factor

Susan R. Heimer,1 Rod A. Welch,2 Nicole T. Perna,3 György Pósfai,4 Peter S. Evans,3 James B. Kaper,1 Fred R. Blattner,3 and Harry L. T. Mobley1*

Department of Microbiology and Immunology, University of Maryland School of Medicine, Baltimore, Maryland 21201,1 Department of Medical MicrobiologyImmunology,2 Laboratory of Genetics, University of Wisconsin Madison, Wisconsin 53706;,3 Institute of Biochemistry, Biological Research Center, Hungarian Academy of Science, Szeged, Hungary 67014

Received 29 June 2001/ Returned for modification 8 October 2001/ Accepted 12 November 2001

Recent genomic analyses of Escherichia coli O157:H7 strain EDL933 revealed two loci encoding urease gene homologues (ureDABCEFG), which are absent in nonpathogenic E. coli strain K-12. This report demonstrates that the cloned EDL933 ure gene cluster is capable of synthesizing urease in an E. coli DH5{alpha} background. However, when the gene fragment is transformed back into the native EDL933 background, the enzymatic activity of the cloned determinants is undetectable. We speculate that an unidentified trans-acting factor in enterohemorrhagic E. coli (EHEC) is responsible for this regulation of ure expression. In addition, Fur-like recognition sites are present in three independent O157:H7 isolates upstream of ureD and ureA. Enzymatic assays confirmed a difference in urease expression of cloned EHEC ure clusters in E. coli MC3100{Delta}fur. Likewise, interruption of fur in O157:H7 isolate IN1 significantly diminished urease activity. We propose that, similar to the function of Fur in regulating the acid response of Salmonella enterica serovar Typhimurium, it modulates urease expression in EHEC, perhaps contributing to the acid tolerance of the organism.

* Corresponding author. Mailing address: Department of Microbiology and Immunology, University of Maryland School of Medicine, 655 W. Baltimore St., Baltimore, MD 21201. Phone: (410) 706-0466. Fax: (410) 706-6751. E-mail: hmobley{at}umaryland.edu.

Editor: V. J. DiRita

Infection and Immunity, February 2002, p. 1027-1031, Vol. 70, No. 2
0019-9567/01/$04.00+0     DOI: 70.2.1027-1031.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.



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