Arf1 is involved in Neisseria meningitidis-induced cortical branched F-actin network reorganization

Cells experience external forces that deform the plasma membrane to which they adapt by reorganizing their actin cytoskeleton. Here, using the extracellular bacterium Neisseria meningitidis as a model system, we explore how this bacterium reorganizes the cortical actin cytoskeleton subsequently to mechanical membrane deformations. Meningococci trigger the formation of tubular cellular plasma membrane protrusions by a previously described adhesion-driven process known as one-dimensional wetting. Cryo-electron tomography reveals that in epithelial cells such a deformation of the plasma membrane leads to the formation of F-actin bundles. In contrast, in endothelial cells a branched F-actin network is formed. By combining high resolution photonic microscopy approaches with genetic and drug perturbations in endothelial cells, we demonstrate that Arp2/3 activity is necessary for forming this branched network. We demonstrate the role of the nucleating-promoting factor N-WASP downstream of Cdc42. Proteomic analyses reveal the contribution of the small GTPase Arf1. Taken together, our results delineate an Arf1-Cdc42-N-WASP-Arp2/3 pathway that links mechanical plasma membrane deformation to the subsequent reorganization of a cortical branched F-actin network in endothelial cells.

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Publication Details

Journal
EMBO Reports
Published
2026-06-25
DOI
https://doi.org/10.1038/s44319-026-00843-z
Primary Topic
Bacterial Infections and Vaccines
Type
article
Field-Weighted Citation Impact
0.00

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article

Arf1 is involved in Neisseria meningitidis-induced cortical branched F-actin network reorganization

Audrey Salles, Gaël Moneron, Guillaume Duménil, Anna Sartori-Rupp et al.
EMBO Reports
Bacterial Infections and Vaccines
article

Arf1 is involved in Neisseria meningitidis-induced cortical branched F-actin network reorganization

Audrey Salles, Gaël Moneron, Guillaume Duménil, Anna Sartori-Rupp, Adeline Mallet, Mariette Matondo, Sylvie Goussard, Magalie Duchateau, Léa Swistak, Daria Bonazzi, Esthel Pénard, Jean-Yves Tinévez, Arthur Charles‐Orszag, Cyril Scandola, Dorian Obino, Stéphane Tachon, Margot Sahnine, Quentin Giai Gianetto, Morgane Crochet
article en

Abstract

Cells experience external forces that deform the plasma membrane to which they adapt by reorganizing their actin cytoskeleton. Here, using the extracellular bacterium Neisseria meningitidis as a model system, we explore how this bacterium reorganizes the cortical actin cytoskeleton subsequently to mechanical membrane deformations. Meningococci trigger the formation of tubular cellular plasma membrane protrusions by a previously described adhesion-driven process known as one-dimensional wetting. Cryo-electron tomography reveals that in epithelial cells such a deformation of the plasma membrane leads to the formation of F-actin bundles. In contrast, in endothelial cells a branched F-actin network is formed. By combining high resolution photonic microscopy approaches with genetic and drug perturbations in endothelial cells, we demonstrate that Arp2/3 activity is necessary for forming this branched network. We demonstrate the role of the nucleating-promoting factor N-WASP downstream of Cdc42. Proteomic analyses reveal the contribution of the small GTPase Arf1. Taken together, our results delineate an Arf1-Cdc42-N-WASP-Arp2/3 pathway that links mechanical plasma membrane deformation to the subsequent reorganization of a cortical branched F-actin network in endothelial cells.

EMBO Reports
Centre National de la Recherche Scientifique (FR), Inserm (FR), Institut Pasteur (FR), Université Paris Cité (FR), Institut Cochin (FR), Dynamique du noyau (FR), University of California, Davis (US)
Agence Nationale de la Recherche, Fondation pour la Recherche Médicale, Institut Pasteur, Université de Paris, European Research Council
Openalex Percentile: Top 9%
Bacterial Infections and Vaccines
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