This Article Full Text (PDF) Other Versions of this Article: IAI.01702-06v1 75/3/1203    most recent Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Reprints and Permissions Copyright Information Books from ASM Press MicrobeWorld Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Bourzac, K. M. Articles by Guillemin, K. Search for Related Content PubMed PubMed Citation Articles by Bourzac, K. M. Articles by Guillemin, K.

 Previous Article

Infect. Immun. doi:10.1128/IAI.01702-06
Copyright (c) 2006, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved.

Helicobacter pylori CagA induces AGS cell elongation through a cell retraction defect that is independent of Cdc42, Rac1 and Arp2/3

Institute of Molecular Biology, University of Oregon, Eugene, Oregon USA

^* To whom correspondence should be addressed. Email: guillemin{at}molbio.uoregon.edu.

	Abstract

Helicobacter pylori, which infects over half the world's population, is a significant risk factor in a spectrum of gastric diseases including peptic ulcers and gastric cancer. Strains of H. pylori that deliver the effector molecule CagA into host cells via a type IV secretion system are associated with more severe disease outcomes. In a tissue culture model of infection, CagA delivery results in a dramatic cellular elongation referred to as the "hummingbird" phenotype which is characterized by long, thin cellular extensions. These actin-based cytoskeletal rearrangements are reminiscent of structures that are regulated by Rho GTPases and the Arp2/3 complex. We tested whether these signaling pathways were important in the H. pylori-induced cell elongation phenotype. Contrary to our expectations, we found these molecules are dispensable for cell elongation. Instead, time-lapse video microscopy revealed that cells infected by cagA+ H. pylori become elongated because they fail to release their back ends during cell locomotion. Consistent with a model in which CagA causes cell elongation by inhibiting the disassembly of adhesive cell contacts at migrating cells' lagging ends, immunohistochemical analysis revealed that focal adhesions complexes persist at the distal tips of elongated cell projections. Thus, our data implicate a different set of signaling molecules in the hummingbird phenotype than those previously suspected.