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Journal of Bacteriology, March 2007, p. 2468-2476, Vol. 189, No. 6
0021-9193/07/$08.00+0 doi:10.1128/JB.01848-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

Department of Microbiology, University of Texas Southwestern Medical Center at Dallas, Dallas, Texas 75390-9048,1 Department of Microbiology and Immunology, University of Texas Medical Branch, Galveston, Texas 77555-1070,2 Department of Agricultural Chemistry, Kinki University, Nakamachi 3327-204, Nara 631-8505, Japan3
Received 10 December 2006/ Accepted 5 January 2007
Enterohemorrhagic Escherichia coli (EHEC) O157:H7 is responsible for worldwide outbreaks of bloody diarrhea, hemorrhagic colitis, and life-threatening hemolytic uremic syndrome. After colonizing the large intestine, EHEC forms attaching and effacing (AE) lesions on intestinal epithelial cells. These lesions cause destruction of the microvilli and elicit actin rearrangement to form pedestals that cup each bacterium individually. EHEC responds to a signal produced by the intestinal microbial flora, autoinducer-3 (AI-3), and the host hormones epinephrine and norepinephrine to activate transcription of the genes involved in AE lesion formation. These three signals, involved in interkingdom communication, are sensed by bacterial sensor kinases. Here we describe a novel two-component system, QseEF (quorum-sensing E. coli regulators E and F), which is part of the AI-3/epinephrine/norepinephrine signaling system. QseE is the sensor kinase and QseF the response regulator. The qseEF genes are cotranscribed, and transcription of qseEF is activated by epinephrine through the QseC sensor. A qseF mutant does not form AE lesions. QseF activates transcription of the gene encoding EspFu, an effector protein translocated to the host cell by the EHEC, which mimics a eukaryotic SH2/SH3 adapter protein to engender actin polymerization during pedestal formation. Expression of the espFu gene from a plasmid restored AE lesion formation to the qseF mutant, suggesting that lack of espFu expression in this mutant was responsible for the loss of pedestal formation. These findings suggest the QseEF is a two-component system involved in the regulation of AE lesion formation by EHEC.
Published ahead of print on 12 January 2007.
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