Apical adhesion of meningococci controls host cell basal traction force through Ancreopodia formation
- 1Institut Pasteur, INSERM U1225, Paris, France
Abstract
Extracellular bacterial pathogens remodel the apical surface of host cells, but whether these local interactions are mechanically transmitted across the cell to the basal extracellular matrix remains unclear. Using a combination of in vitro infection models, high-resolution imaging, traction force microscopy and bacterial genetics, we show that Neisseria meningitidis (Nm) adhesion to endothelial cells triggers a rapid increase in traction forces and localized, colony-associated traction-force hotspots on the extracellular matrix. Formation of these hotspots is associated with a novel actin-rich structure, which we term ancreopodia, that links apical bacterial colonies to the basal substrate. Super-resolution microscopy revealed ancreopodia spanning the cell thickness, connecting apical cortical plaques to reorganized basal stress fibers and focal-adhesion components. Dynamic imaging demonstrated coordinated movements of bacterial colonies and basal mechanosensitive proteins, while analysis of pili mutants showed that pilus retraction is required to focus traction forces beneath colonies. Disruption of branched actin assembly or myosin-II activity likewise impaired apico-basal organization and vinculin recruitment. Functionally, Nm infection enhanced local anchoring while restricting single-cell migration and collective endothelial dynamics. Together, these findings identify ancreopodia as a vertical mechanotransduction structure through which an extracellular pathogen couples apical adhesion to basal force transmission and reshapes host-cell mechanics.
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BibTeX
@misc{narayana2026apical,
title = {{Apical adhesion of meningococci controls host cell basal traction force through Ancreopodia formation}},
author = {G. H. N. SANKARA NARAYANA and S. Goussard and J.-Y. Tinevez and G. Dumenil and D. Bonazzi},
howpublished = {bioRxiv},
year = {2026},
month = sep,
doi = {10.64898/2026.09.29.754870},
url = {https://www.biorxiv.org/content/10.64898/2026.09.29.754870v1},
note = {CC BY-NC-ND},
}
RIS
TY - UNPB
TI - Apical adhesion of meningococci controls host cell basal traction force through Ancreopodia formation
AU - G. H. N. SANKARA NARAYANA
AU - S. Goussard
AU - J.-Y. Tinevez
AU - G. Dumenil
AU - D. Bonazzi
PY - 2026
DA - 2026/09/29
PB - bioRxiv
DO - 10.64898/2026.09.29.754870
UR - https://www.biorxiv.org/content/10.64898/2026.09.29.754870v1
AB - Extracellular bacterial pathogens remodel the apical surface of host cells, but whether these local interactions are mechanically transmitted across the cell to the basal extracellular matrix remains unclear. Using a combination of in vitro infection models, high-resolution imaging, traction force microscopy and bacterial genetics, we show that Neisseria meningitidis (Nm) adhesion to endothelial cells triggers a rapid increase in traction forces and localized, colony-associated traction-force hotspots on the extracellular matrix. Formation of these hotspots is associated with a novel actin-rich structure, which we term ancreopodia, that links apical bacterial colonies to the basal substrate. Super-resolution microscopy revealed ancreopodia spanning the cell thickness, connecting apical cortical plaques to reorganized basal stress fibers and focal-adhesion components. Dynamic imaging demonstrated coordinated movements of bacterial colonies and basal mechanosensitive proteins, while analysis of pili mutants showed that pilus retraction is required to focus traction forces beneath colonies. Disruption of branched actin assembly or myosin-II activity likewise impaired apico-basal organization and vinculin recruitment. Functionally, Nm infection enhanced local anchoring while restricting single-cell migration and collective endothelial dynamics. Together, these findings identify ancreopodia as a vertical mechanotransduction structure through which an extracellular pathogen couples apical adhesion to basal force transmission and reshapes host-cell mechanics.
ER -