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<p>Cells experience external forces that deform the plasma membrane to which they adapt by reorganizing their actin cytoskeleton. Here, using the extracellular bacterium <i>Neisseria meningitidis</i> 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.</p>

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

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年6月25日

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

摘要

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.