This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowReprints and Permissions
Right arrow Copyright Information
Right arrow Books from ASM Press
Right arrow MicrobeWorld
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Reading, N. C.
Right arrow Articles by Sperandio, V.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Reading, N. C.
Right arrow Articles by Sperandio, V.

 Previous Article  |  Next Article 

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.

A Novel Two-Component Signaling System That Activates Transcription of an Enterohemorrhagic Escherichia coli Effector Involved in Remodeling of Host Actin{triangledown}

Nicola C. Reading,1 Alfredo G. Torres,2 Melissa M. Kendall,1 David T. Hughes,1 Kaneyoshi Yamamoto,3 and Vanessa Sperandio1*

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.

* Corresponding author. Mailing address: University of Texas Southwestern Medical Center, Dept. of Microbiology, 5323 Harry Hines Blvd., Dallas, TX 75390-9048. Phone: (214) 648-1603. Fax: (214) 648-5905. E-mail: vanessa.sperandio{at}utsouthwestern.edu.

{triangledown} Published ahead of print on 12 January 2007.

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.



This article has been cited by other articles:

  • Reading, N. C., Rasko, D. A., Torres, A. G., Sperandio, V. (2009). The two-component system QseEF and the membrane protein QseG link adrenergic and stress sensing to bacterial pathogenesis. Proc. Natl. Acad. Sci. USA 106: 5889-5894 [Abstract] [Full Text]  
  • Iguchi, A., Thomson, N. R., Ogura, Y., Saunders, D., Ooka, T., Henderson, I. R., Harris, D., Asadulghani, M., Kurokawa, K., Dean, P., Kenny, B., Quail, M. A., Thurston, S., Dougan, G., Hayashi, T., Parkhill, J., Frankel, G. (2009). Complete Genome Sequence and Comparative Genome Analysis of Enteropathogenic Escherichia coli O127:H6 Strain E2348/69. J. Bacteriol. 191: 347-354 [Abstract] [Full Text]  
  • Oneal, M. J., Schafer, E. R., Madsen, M. L., Minion, F. C. (2008). Global transcriptional analysis of Mycoplasma hyopneumoniae following exposure to norepinephrine. Microbiology 154: 2581-2588 [Abstract] [Full Text]  
  • Ryan, R. P., Dow, J. M. (2008). Diffusible signals and interspecies communication in bacteria. Microbiology 154: 1845-1858 [Abstract] [Full Text]  
  • Jelcic, I., Hufner, E., Schmidt, H., Hertel, C. (2008). Repression of the Locus of the Enterocyte Effacement-Encoded Regulator of Gene Transcription of Escherichia coli O157:H7 by Lactobacillus reuteri Culture Supernatants Is LuxS and Strain Dependent. Appl. Environ. Microbiol. 74: 3310-3314 [Abstract] [Full Text]  
  • Garcia-Angulo, V. A., Deng, W., Thomas, N. A., Finlay, B. B., Puente, J. L. (2008). Regulation of Expression and Secretion of NleH, a New Non-Locus of Enterocyte Effacement-Encoded Effector in Citrobacter rodentium. J. Bacteriol. 190: 2388-2399 [Abstract] [Full Text]  
  • Kendall, M. M., Rasko, D. A., Sperandio, V. (2007). Global Effects of the Cell-to-Cell Signaling Molecules Autoinducer-2, Autoinducer-3, and Epinephrine in a luxS Mutant of Enterohemorrhagic Escherichia coli. Infect. Immun. 75: 4875-4884 [Abstract] [Full Text]  
  • Mellies, J. L., Barron, A. M. S., Carmona, A. M. (2007). Enteropathogenic and Enterohemorrhagic Escherichia coli Virulence Gene Regulation. Infect. Immun. 75: 4199-4210 [Full Text]  


Copyright © 2009 by the American Society for Microbiology.   For an alternate route to Journals.ASM.org, visit: http://intl-journals.asm.org | More Info»