ArticleCell reports2020
Shigella flexneri Disruption of Cellular Tension Promotes Intercellular Spread.
Article in Cell reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 36 citations in OpenAlex.
- Role of the Host Membrane Trafficking Protein Dynamin 2 in Cell-to-Cell Spread of Bacterial Pathogens.Cells · 2026Review
- Exploring microorganism-host interactions: Emerging organoid models and analytical approaches.mLife · 2026Review
- ThemSphere · 2025Article
- Article
- Host PIK3C3 promotes Shigella flexneri spread from cell to cell through vacuole formation.PLoS pathogens · 2025Article
- The Human-Specific miR-6762-5p Is an Activator of RhoA GTPase Enhancing Shigella flexneri Intercellular Spreading.Molecular microbiology · 2025Article
- ThemBio · 2025Article
- A flexible peptide linking the periplasmic and cytoplasmic domains of MxiG controls type III secretion signaling and stable sorting platform assembly inFrontiers in cellular and infection microbiology · 2025Article
- A RecombinantInternational journal of molecular sciences · 2024Article
- The host GTPase Dynamin 2 modulates apical junction structure to control cell-to-cell spread ofInfection and immunity · 2024Article
- Pushing boundaries: mechanisms enabling bacterial pathogens to spread between cells.Infection and immunity · 2024Review
- PathogenicJournal of bacteriology · 2024Review
- Geometric constraint-triggered collagen expression mediates bacterial-host adhesion.Nature communications · 2023Article
- Manipulation of host cell plasma membranes by intracellular bacterial pathogens.Current opinion in microbiology · 2023Review
- Mechanical Forces Govern Interactions of Host Cells with Intracellular Bacterial Pathogens.Microbiology and molecular biology reviews : MMBR · 2022Review
- The type 3 secretion effector IpgD promotes S. flexneri dissemination.PLoS pathogens · 2022Article
- The T3SS ofMicroorganisms · 2020Review
- Review
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
During infection, some bacterial pathogens invade the eukaryotic cytosol and spread between cells of an epithelial monolayer. Intercellular spread occurs when these pathogens push against the plasma membrane, forming protrusions that are engulfed by adjacent cells. Here, we show that IpaC, a Shigella flexneri type 3 secretion system protein, binds the host cell-adhesion protein β-catenin and facilitates efficient protrusion formation. S. flexneri producing a point mutant of IpaC that cannot interact with β-catenin is defective in protrusion formation and spread. Spread is restored by chemical reduction of intercellular tension or genetic depletion of β-catenin, and the magnitude of the protrusion defect correlates with membrane tension, indicating that IpaC reduces membrane tension, which facilitates protrusion formation. IpaC stabilizes adherens junctions and does not alter β-catenin localization at the membrane. Thus, Shigella, like other bacterial pathogens, reduces intercellular tension to efficiently spread between cells.
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Registered trials
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