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Infection and Immunity, April 2008, p. 1465-1475, Vol. 76, No. 4
0019-9567/08/$08.00+0     doi:10.1128/IAI.01265-07
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

Activation of the Cpx Envelope Stress Response Down-Regulates Expression of Several Locus of Enterocyte Effacement-Encoded Genes in Enteropathogenic Escherichia coli{triangledown}

Dawn M. MacRitchie,1 Jordan D. Ward,2 Anna Z. Nevesinjac,1 and Tracy L. Raivio1*

Department of Biological Sciences, University of Alberta, Edmonton, Alberta, Canada T6G 2E9,1 Cancer Research UK, London Research Institute, Clare Hall Laboratories, Blanche Lane, South Mimms EN6 3LD, United Kingdom2

Received 14 September 2007/ Returned for modification 14 October 2007/ Accepted 16 January 2008

The Cpx two-component system regulates an extracytoplasmic stress response that functions to rid the envelope of misfolded and mislocalized proteins that may interfere with normal cellular processes. The Cpx pathway is also involved in pathogenesis. This study investigated the role of the Cpx response in enteropathogenic Escherichia coli (EPEC) type III secretion (T3S). It was determined that a functional Cpx pathway is not required for T3S but that pathway activation inhibits secretion by reducing the cellular pools of T3S substrates. The EPEC T3S system structural components, as well as a number of its substrates, are encoded on the locus of enterocyte effacement (LEE) pathogenicity island. Transcriptional fusions to the five major operons of the LEE were constructed and examined under Cpx pathway-activating conditions. Induction of the Cpx response caused a decrease in the transcription of several LEE operons, with the most pronounced effect on LEE4 and LEE5. Collectively, these two operons encode components of the T3S translocation apparatus, the bacterial adhesin intimin, and the translocated bacterial receptor Tir. These data show for the first time that activation of the Cpx envelope stress response in EPEC inhibits T3S of both translocators and effectors, likely through down regulation of LEE transcription. Coupled with recent findings, our results suggest that Cpx-mediated down regulation of virulence is a conserved theme in a number of bacterial pathogens.

* Corresponding author. Mailing address: Department of Biological Sciences, University of Alberta, CW405 Biological Sciences Building, Edmonton, Alberta, Canada T6G 2E9. Phone: (780) 492-3491. Fax: (780) 492-9234. E-mail: traivio{at}ualberta.ca

{triangledown} Published ahead of print on 28 January 2008.

Editor: J. B. Bliska

Infection and Immunity, April 2008, p. 1465-1475, Vol. 76, No. 4
0019-9567/08/$08.00+0     doi:10.1128/IAI.01265-07
Copyright © 2008, American Society for Microbiology. All Rights Reserved.



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