Actin pedestal formation by enteropathogenic Escherichia coli and intracellular motility of Shigella flexneri are abolished in N-WASP-defective cells

Tools

Item Type:	Article
Title:	Actin pedestal formation by enteropathogenic Escherichia coli and intracellular motility of Shigella flexneri are abolished in N-WASP-defective cells
Creators Name:	Lommel, S., Benesch, S., Rottner, K., Franz, T., Wehland, J. and Kühn, R.
Abstract:	In mammalian cells, actin dynamics is tightly controlled through small GTPases of the Rho family, WASP/Scar proteins and the Arp2/3 complex. We employed Cre/loxP-mediated gene targeting to disrupt the ubiquitously expressed N-WASP in the mouse germline, which led to embryonic lethality. To elucidate the role of N-WASP at the cellular level, we immortalized embryonic fibroblasts and selected various N-WASP-defective cell lines. These fibroblasts showed no apparent morphological alterations and were highly responsive to the induction of filopodia, but failed to support the motility of Shigella flexneri. In addition, enteropathogenic Escherichia coli were incapable of inducing the formation of actin pedestals in N-WASP-defective cells. Our results prove the essential role of this protein for actin cytoskeletal changes induced by these bacterial pathogens in vivo and in addition show for the first time that N-WASP is dispensable for filopodia formation.
Keywords:	Actins, Alleles, Bacterial Physiological Phenomena, Southern Blotting, Cell Line, Cultured Cells, Complementary DNA, Escherichia coli, Fibroblasts, Computer-Assisted Image Processing, Fluorescence Microscopy, Genetic Models, Molecular Sequence Data, Nerve Tissue Proteins, Protein Binding, Pseudopodia, Reverse Transcriptase Polymerase Chain Reaction, Shigella flexneri, Neuronal Wiskott-Aldrich Syndrome Protein, cdc42 GTP-Binding Protein, Animals, Mice
Source:	EMBO Reports
ISSN:	1469-221X
Publisher:	Oxford University Press
Volume:	2
Number:	9
Page Range:	850-857
Date:	September 2001
Official Publication:	https://doi.org/10.1093/embo-reports/kve197
PubMed:	View item in PubMed

Repository Staff Only: item control page