Sign up for Table of Contents Alerts!
Email this page
Print this page
Article Addendum
The Autophagic Pathway: A Cell Survival Strategy Against the Bacterial Pore-Forming Toxin Vibrio Cholerae Cytolysin
Héctor A. Saka, Maximiliano G. Gutiérrez, José L. Bocco and María I. Colombo
volume 3 | issue 4
July/August 2007Pages: 363 - 365
We now provide open access to journal articles published online for one year or more. This article may be downloaded at the following link:
Download PDF If the document does not open, please right-click on the link (control-click on a Macintosh) and select the option to save the file to disk.
Vibrio cholerae is the causative agent of cholera in humans. In addition to the critical virulence factors cholera toxin and toxin co-regulated pilus, V. cholerae secretes V. cholerae cytolysin (VCC), a pore-forming exotoxin able to induce cell lysis and extensive vacuolation. We have shown that this vacuolation is related to the activation of autophagy in response to VCC action. Furthermore, we found that the autophagic pathway was required to protect cells upon VCC intoxication. Based on additional data presented here, we propose a model aimed to explain the mechanism of cell protection. We postulate that VCC-induced autophagic vacuoles, which display features of multivesicular bodies and enclose the toxin, are implicated in cell defense through VCC degradation involving fusion with lysosomes.
Addendum to:
Protective Role of Autophagy Against Vibrio cholerae Cytolysin, a Pore-Forming Toxin from V. cholerae
M.G. Gutierrez, H.A. Saka, I. Chinen, F.C.M. Zoppino, T. Yoshimori, J.L. Bocco and M.I. Colombo
Proc Natl Acad Sci USA 2007; 104:1829-34
Authors
Héctor A. Saka
Universidad Nacional de Córdoba
Maximiliano G. Gutiérrez
The European Molecular Biology Laboratory
José L. Bocco
Universidad Nacional de Córdoba
María I. Colombo
Laboratorio de Biología Celular y Molecular; Instituto de Histología y Embriología (IHEM); Facultad de Ciencias Médicas; Universidad Nacional de Cuyo-CONICET; Mendoza Argentina
We now provide open access to journal articles published online for one year or more. This article may be downloaded at the following link:
Download PDF If the document does not open, please right-click on the link (control-click on a Macintosh) and select the option to save the file to disk.