Bacterial toxins modifying the actin cytoskeleton Authors Jean-François Richard Institut des Neurosciences, Université Pierre et Marie Curie, CNRS UMR7624, Paris, France Laetitia Petit Unité des Toxines Microbiennes, Institut Pasteur, Paris, France Maryse Gibert Unité des Toxines Microbiennes, Institut Pasteur, Paris, France Jean Christophe Marvaud Unité des Toxines Microbiennes, Institut Pasteur, Paris, France Claude Bouchaud Unité des Toxines Microbiennes, Institut Pasteur, Paris, France Michel R. Popoff Unité des Toxines Microbiennes, Institut Pasteur, Paris, France Keywords: toxins, actin, rho proteins, ras proteins, intercellular junction Abstract Numerous bacterial toxins recognize the actin cytoskeleton as a target. The clostridial binary toxins (Iota and C2 families) ADP-ribosylate the actin monomers causing the dissociation of the actin filaments. The large clostridial toxins from Clostridium difficile, Clostridium sordellii and Clostridium novyi inactivate, by glucosylation, proteins from the Rho family that regulate actin polymerization. In contrast, the cytotoxic necrotic factor from Escherichia coli activates Rho by deamidation and increases the formation of actin filaments. The enterotoxin of Bacteroides fragilis is a protease specific for E-cadherin and it promotes the reorganization of the actin cytoskeleton. The bacterial toxins that modify the actin cytoskeleton induce various cell disfunctions including changes in cell barrier permeability and disruption of intercellular junctions. Downloads PDF Published 2010-03-16 Issue Vol. 2 No. 3 (1999) Section Review Articles License Submission of a manuscript to International Microbiology implies: that the work described has not been published before, including publication in the World Wide Web (except in the form of an Abstract or as part of a published lecture, review, or thesis); that it is not under consideration for publication elsewhere; that all the coauthors have agreed to its publication. The corresponding author signs for and accepts responsability for releasing this material and will act on behalf of any and all coauthors regarding the editorial review and publication process.If an article is accepted for publication in International Microbiology, the authors (or other copyright holder) must transfer to the journal the right–not exclusive–to reproduce and distribute the article including reprints, translations, photographic reproductions, microform, electronic form (offline, online) or any other reproductions of similar nature. Nevertheless, all article in International Microbiology will be available on the Internet to any reader at no cost. The journal allows users to freely download, copy, print, distribute, search, and link to the full text of any article, provided the authorship and source of the published article is cited. The copyright owner's consent does not include copying for new works, or resale. In these cases, the specific written permission of International Microbiology must first be obtained.Authors are requested to create a link to the published article on the journal's website. The link must be accompanied by the following text: "The original publication is available on LINK at <http://www.im.microbios.org>. Please use the appropiate URL for the article in LINK. Articles disseminated via LINK are indexed, abstracted, and referenced by many abstracting and information services, bibliographic networks, subscription agencies, library networks, and consortia.