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 Taylor, K. A.
Right arrow Articles by Donnenberg, M. S.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Taylor, K. A.
Right arrow Articles by Donnenberg, M. S.

 Previous Article  |  Next Article 

Infection and Immunity, January 1999, p. 120-125, Vol. 67, No. 1
0019-9567/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.

Expression of the EspB Protein of Enteropathogenic Escherichia coli within HeLa Cells Affects Stress Fibers and Cellular Morphology

Kathleen A. Taylor,1 Paul W. Luther,2 and Michael S. Donnenberg1,*

Division of Infectious Diseases, Department of Medicine,1 and Department of Physiology,2 University of Maryland School of Medicine, Baltimore, Maryland 21201

Received 13 July 1998/Returned for modification 6 October 1998/Accepted 28 October 1998

The EspB protein of enteropathogenic Escherichia coli (EPEC) is essential for the signaling events that lead to the accumulation of actin beneath intimately attached bacteria, a process that is known as the attaching and effacing effect. EspB is targeted to the host cell cytoplasm by a type III secretion apparatus. To determine the effect of intracellular EspB on the host cell cytoskeleton, we transfected HeLa cells with a plasmid containing the espB gene under the control of an inducible eukaryotic promoter. A HeLa cell clone that expressed espB mRNA and EspB protein after induction was selected for further study. The expression of EspB in these cells caused a dramatic change in cell morphology and a marked reduction in actin stress fibers. Cells expressing EspB were significantly impaired in their ability to support invasion by EPEC and Salmonella typhimurium. However, the expression of EspB within host cells could not compensate for the lack of EspB expression by an espB mutant strain of EPEC to restore attaching and effacing activity. These studies suggest that EspB is a cytoskeletal toxin that is translocated to the host cell cytoplasm, where it causes a redistribution of actin.


* Corresponding author. Mailing address: Division of Infectious Diseases, University of Maryland School of Medicine, 10 South Pine St., MSTF 900, Baltimore, MD 21201. Phone: (410) 706-7560. Fax: (410) 706-8700. E-mail: mdonnenb{at}umaryland.edu.


Infection and Immunity, January 1999, p. 120-125, Vol. 67, No. 1
0019-9567/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.



This article has been cited by other articles:

  • Bellmeyer, A., Cotton, C., Kanteti, R., Koutsouris, A., Viswanathan, V. K., Hecht, G. (2009). Enterohemorrhagic Escherichia coli suppresses inflammatory response to cytokines and its own toxin. Am. J. Physiol. Gastrointest. Liver Physiol. 297: G576-G581 [Abstract] [Full Text]  
  • Luo, W., Donnenberg, M. S. (2006). Analysis of the Function of Enteropathogenic Escherichia coli EspB by Random Mutagenesis. Infect. Immun. 74: 810-820 [Abstract] [Full Text]  
  • Rodriguez-Escudero, I., Hardwidge, P. R., Nombela, C., Cid, V. J., Finlay, B. B., Molina, M. (2005). Enteropathogenic Escherichia coli type III effectors alter cytoskeletal function and signalling in Saccharomyces cerevisiae. Microbiology 151: 2933-2945 [Abstract] [Full Text]  
  • Garmendia, J., Frankel, G., Crepin, V. F. (2005). Enteropathogenic and Enterohemorrhagic Escherichia coli Infections: Translocation, Translocation, Translocation. Infect. Immun. 73: 2573-2585 [Full Text]  
  • Shaw, R. K, Cleary, J., Murphy, M. S., Frankel, G., Knutton, S. (2005). Interaction of Enteropathogenic Escherichia coli with Human Intestinal Mucosa: Role of Effector Proteins in Brush Border Remodeling and Formation of Attaching and Effacing Lesions. Infect. Immun. 73: 1243-1251 [Abstract] [Full Text]  
  • Gartner, J. F., Schmidt, M. A. (2004). Comparative Analysis of Locus of Enterocyte Effacement Pathogenicity Islands of Atypical Enteropathogenic Escherichia coli. Infect. Immun. 72: 6722-6728 [Abstract] [Full Text]  
  • Knappstein, S., Ide, T., Schmidt, M. A., Heusipp, G. (2004). {alpha}1-Antitrypsin Binds to and Interferes with Functionality of EspB from Atypical and Typical Enteropathogenic Escherichia coli Strains. Infect. Immun. 72: 4344-4350 [Abstract] [Full Text]  
  • Campellone, K. G., Rankin, S., Pawson, T., Kirschner, M. W., Tipper, D. J., Leong, J. M. (2004). Clustering of Nck by a 12-residue Tir phosphopeptide is sufficient to trigger localized actin assembly. JCB 164: 407-416 [Abstract] [Full Text]  
  • Clarke, S. C., Haigh, R. D., Freestone, P. P. E., Williams, P. H. (2003). Virulence of Enteropathogenic Escherichia coli, a Global Pathogen. Clin. Microbiol. Rev. 16: 365-378 [Abstract] [Full Text]  
  • Neves, B. C., Mundy, R., Petrovska, L., Dougan, G., Knutton, S., Frankel, G. (2003). CesD2 of Enteropathogenic Escherichia coli Is a Second Chaperone for the Type III Secretion Translocator Protein EspD. Infect. Immun. 71: 2130-2141 [Abstract] [Full Text]  
  • Hauf, N., Chakraborty, T. (2003). Suppression of NF-{kappa}B Activation and Proinflammatory Cytokine Expression by Shiga Toxin-Producing Escherichia coli. J. Immunol. 170: 2074-2082 [Abstract] [Full Text]  
  • Kenny, B. (2002). Enteropathogenic Escherichia coli (EPEC) - a crafty subversive little bug. Microbiology 148: 1967-1978 [Full Text]  
  • Nougayrede, J.-P., Boury, M., Tasca, C., Marches, O., Milon, A., Oswald, E., De Rycke, J. (2001). Type III Secretion-Dependent Cell Cycle Block Caused in HeLa Cells by Enteropathogenic Escherichia coli O103. Infect. Immun. 69: 6785-6795 [Abstract] [Full Text]  
  • Hecht, G. (2001). Microbes and Microbial Toxins: Paradigms for Microbial-Mucosal Interactions: VII. Enteropathogenic Escherichia coli: physiological alterations from an extracellular position. Am. J. Physiol. Gastrointest. Liver Physiol. 281: G1-G7 [Abstract] [Full Text]  
  • Daniell, S. J., Delahay, R. M., Shaw, R. K., Hartland, E. L., Pallen, M. J., Booy, F., Ebel, F., Knutton, S., Frankel, G. (2001). Coiled-Coil Domain of Enteropathogenic Escherichia coli Type III Secreted Protein EspD Is Involved in EspA Filament-Mediated Cell Attachment and Hemolysis. Infect. Immun. 69: 4055-4064 [Abstract] [Full Text]  
  • Vallance, B. A., Finlay, B. B. (2000). Exploitation of host cells by enteropathogenic Escherichiacoli. Proc. Natl. Acad. Sci. USA 97: 8799-8806 [Abstract] [Full Text]  
  • Tacket, C. O., Sztein, M. B., Losonsky, G., Abe, A., Finlay, B. B., McNamara, B. P., Fantry, G. T., James, S. P., Nataro, J. P., Levine, M. M., Donnenberg, M. S. (2000). Role of EspB in Experimental Human Enteropathogenic Escherichia coli Infection. Infect. Immun. 68: 3689-3695 [Abstract] [Full Text]