Actin Cytoskeleton Manipulation by Effector Proteins Secreted by Diarrheagenic Escherichia coli PathotypesReport as inadecuate

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BioMed Research InternationalVolume 2013 2013, Article ID 374395, 22 pages

Review ArticleDepartment of Cell Biology, Centro de Investigación y de Estudios Avanzados del IPN CINVESTAV-IPN, Apartado Postal 14-740, 07000 México, DF, Mexico

Received 24 August 2012; Accepted 22 October 2012

Academic Editor: Gad Frankel

Copyright © 2013 Fernando Navarro-Garcia et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


The actin cytoskeleton is a dynamic structure necessary for cell and tissue organization, including the maintenance of epithelial barriers. Disruption of the epithelial barrier coincides with alterations of the actin cytoskeleton in several disease states. These disruptions primarily affect the paracellular space, which is normally regulated by tight junctions. Thereby, the actin cytoskeleton is a common and recurring target of bacterial virulence factors. In order to manipulate the actin cytoskeleton, bacteria secrete and inject toxins and effectors to hijack the host cell machinery, which interferes with host-cell pathways and with a number of actin binding proteins. An interesting model to study actin manipulation by bacterial effectors is Escherichia coli since due to its genome plasticity it has acquired diverse genetic mobile elements, which allow having different E. coli varieties in one bacterial species. These E. coli pathotypes, including intracellular and extracellular bacteria, interact with epithelial cells, and their interactions depend on a specific combination of virulence factors. In this paper we focus on E. coli effectors that mimic host cell proteins to manipulate the actin cytoskeleton. The study of bacterial effector-cytoskeleton interaction will contribute not only to the comprehension of the molecular causes of infectious diseases but also to increase our knowledge of cell biology.

Author: Fernando Navarro-Garcia, Antonio Serapio-Palacios, Paul Ugalde-Silva, Gabriela Tapia-Pastrana, and Lucia Chavez-Dueñas



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