Arf1 is involved in Neisseria meningitidis-induced cortical branched F-actin network reorganization
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.
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BibTeX
@article{sahnine2026arf1,
title = {{Arf1 is involved in Neisseria meningitidis-induced cortical branched F-actin network reorganization}},
author = {Margot Sahnine and Morgane Crochet and Stéphane Tachon and Sylvie Goussard and Esthel Pénard and Cyril Scandola and Magalie Duchateau and Quentin Giai Gianetto and Audrey Salles and Gaël Moneron and Léa Swistak and Arthur Charles-Orszag and Adeline Mallet and Mariette Matondo and Jean-Yves Tinevez and Daria Bonazzi and Anna Sartori-Rupp and Guillaume Duménil and Dorian Obino},
journal = {EMBO Reports},
year = {2026},
month = jun,
doi = {10.1038/s44319-026-00843-z},
url = {https://hal.science/hal-05785011v1},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - Arf1 is involved in Neisseria meningitidis-induced cortical branched F-actin network reorganization
AU - Margot Sahnine
AU - Morgane Crochet
AU - Stéphane Tachon
AU - Sylvie Goussard
AU - Esthel Pénard
AU - Cyril Scandola
AU - Magalie Duchateau
AU - Quentin Giai Gianetto
AU - Audrey Salles
AU - Gaël Moneron
AU - Léa Swistak
AU - Arthur Charles-Orszag
AU - Adeline Mallet
AU - Mariette Matondo
AU - Jean-Yves Tinevez
AU - Daria Bonazzi
AU - Anna Sartori-Rupp
AU - Guillaume Duménil
AU - Dorian Obino
PY - 2026
DA - 2026/06/25
JO - EMBO Reports
DO - 10.1038/s44319-026-00843-z
UR - https://hal.science/hal-05785011v1
AB - 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.
SN - 1469-221X
SN - 1469-3178
ER -