ArticlePLoS pathogens2019
Activation of Shigella flexneri type 3 secretion requires a host-induced conformational change to the translocon pore.
Article in PLoS pathogens, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed.
- Article
- Development of themSphere · 2023Article
- Recent insights into type-3 secretion system injectisome structure and mechanism of human enteric pathogens.Current opinion in microbiology · 2023Review
- Article
- Type III secretion by Yersinia pseudotuberculosis is reliant upon an authentic N-terminal YscX secretor domain.Molecular microbiology · 2022Article
- The type 3 secretion system requires actin polymerization to open translocon pores.PLoS pathogens · 2021Article
- TheMicroorganisms · 2021Review
- Cell-type-specific hypertranslocation of effectors by the Pseudomonas aeruginosa type III secretion system.Molecular microbiology · 2021Article
- Structural Insights ofFrontiers in cellular and infection microbiology · 2021Article
- The T3SS ofMicroorganisms · 2020Review
- Article
- Staying out or Going in? The Interplay between Type 3 and Type 5 Secretion Systems in Adhesion and Invasion of Enterobacterial Pathogens.International journal of molecular sciences · 2020Review
Corrections and comments
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Authors and funding
5 authors.
Funding
Abstract
Type 3 secretion systems (T3SSs) are conserved bacterial nanomachines that inject virulence proteins (effectors) into eukaryotic cells during infection. Due to their ability to inject heterologous proteins into human cells, these systems are being developed as therapeutic delivery devices. The T3SS assembles a translocon pore in the plasma membrane and then docks onto the pore. Docking activates effector secretion through the pore and into the host cytosol. Here, using Shigella flexneri, a model pathogen for the study of type 3 secretion, we determined the molecular mechanisms by which host intermediate filaments trigger docking and enable effector secretion. We show that the interaction of intermediate filaments with the translocon pore protein IpaC changed the pore's conformation in a manner that was required for docking. Intermediate filaments repositioned residues of the Shigella pore protein IpaC that are located on the surface of the pore and in the pore channel. Restricting these conformational changes blocked docking in an intermediate filament-dependent manner. These data demonstrate that a host-induced conformational change to the pore enables T3SS docking and effector secretion, providing new mechanistic insight into the regulation of type 3 secretion.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.