ArticleNature communications2024
Microtubules provide force to promote membrane uncoating in vacuolar escape for a cyto-invasive bacterial pathogen.
Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Review
- ThebioRxiv : the preprint server for biology · 2026Article
- Identification of TPRA1 as a Novel Receptor and Predictive Biomarker for Oncolytic Virus M1.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- The intracellular bacterium Orientia tsutsugamushi uses the autotransporter ScaC to activate BICD adaptors for dynein-based motility.Nature communications · 2025Article
- Pathogen-induced rerouting of host membrane trafficking.Current opinion in cell biology · 2025Review
- The bacterial type three secretion system induces mechanoporation of vacuolar membranes.PLoS biology · 2025Article
Corrections and comments
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Authors and funding
8 authors.
Funding
Abstract
Intracellular bacterial pathogens gain entry to mammalian cells inside a vacuole derived from the host membrane. Some of them escape the bacteria-containing vacuole (BCV) and colonize the cytosol. Bacteria replicating within BCVs coopt the microtubule network to position it within infected cells, whereas the role of microtubules for cyto-invasive pathogens remains obscure. Here, we show that the microtubule motor cytoplasmic dynein-1 and specific activating adaptors are hijacked by the enterobacterium Shigella flexneri. These host proteins were found on infection-associated macropinosomes (IAMs) formed during Shigella internalization. We identified Rab8 and Rab13 as mediators of dynein recruitment and discovered that the Shigella effector protein IpaH7.8 promotes Rab13 retention on moving BCV membrane remnants, thereby facilitating membrane uncoating of the Shigella-containing vacuole. Moreover, the efficient unpeeling of BCV remnants contributes to a successful intercellular spread. Taken together, our work demonstrates how a bacterial pathogen subverts the intracellular transport machinery to secure a cytosolic niche.
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