Evidence map›Paper›PMID 32866204›Full record

ArticlePLoS pathogens2020

Shigella hijacks the exocyst to cluster macropinosomes for efficient vacuolar escape.

Yuen-Yan Chang, Virginie Stévenin, Magalie Duchateau, Quentin Giai Gianetto, Veronique Hourdel, Cristina Dias Rodrigues, Mariette Matondo, Norbert Reiling, Jost Enninga

Open access · goldAbstract read
In one paragraph

Article in PLoS pathogens, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
4.4field-weighted citation impact, top 6% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

16 citing papers in PubMed, 37 citations in OpenAlex.

  1. Review
  2. Pathogen-induced rerouting of host membrane trafficking.Current opinion in cell biology · 2025
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  12. Modification of phosphoinositides by theFrontiers in cellular and infection microbiology · 2022
    Review
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors at 2 institutions in 2 countries.

Yuen-Yan ChangDynamics of Host-Pathogen Interactions Unit and CNRS UMR3691, Institut Pasteur, Paris, France.
Virginie StéveninDynamics of Host-Pathogen Interactions Unit and CNRS UMR3691, Institut Pasteur, Paris, France.ORCID 0000-0003-1303-4085
Magalie DuchateauMass Spectrometry for Biology Unit, Proteomics Platform, Institut Pasteur, USR CNRS, Paris, France.ORCID 0000-0001-5475-3065
Quentin Giai GianettoMass Spectrometry for Biology Unit, Proteomics Platform, Institut Pasteur, USR CNRS, Paris, France.ORCID 0000-0001-6815-2498
Veronique HourdelMass Spectrometry for Biology Unit, Proteomics Platform, Institut Pasteur, USR CNRS, Paris, France.
Cristina Dias RodriguesDynamics of Host-Pathogen Interactions Unit and CNRS UMR3691, Institut Pasteur, Paris, France.
Mariette MatondoMass Spectrometry for Biology Unit, Proteomics Platform, Institut Pasteur, USR CNRS, Paris, France.ORCID 0000-0003-3958-7710
Norbert ReilingMicrobial Interface Biology, Research Center Borstel, Leibniz Lung Center, Borstel, Germany.ORCID 0000-0001-6673-4291
Jost EnningaDynamics of Host-Pathogen Interactions Unit and CNRS UMR3691, Institut Pasteur, Paris, France.ORCID 0000-0002-5218-349X
Centre National de la Recherche Scientifique · FRGerman Center for Infection Research · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Shigella flexneri invades host cells by entering within a bacteria-containing vacuole (BCV). In order to establish its niche in the host cytosol, the bacterium ruptures its BCV. Contacts between S. flexneri BCV and infection-associated macropinosomes (IAMs) formed in situ have been reported to enhance BCV disintegration. The mechanism underlying S. flexneri vacuolar escape remains however obscure. To decipher the molecular mechanism priming the communication between the IAMs and S. flexneri BCV, we performed mass spectrometry-based analysis of the magnetically purified IAMs from S. flexneri-infected cells. While proteins involved in host recycling and exocytic pathways were significantly enriched at the IAMs, we demonstrate more precisely that the S. flexneri type III effector protein IpgD mediates the recruitment of the exocyst to the IAMs through the Rab8/Rab11 pathway. This recruitment results in IAM clustering around S. flexneri BCV. More importantly, we reveal that IAM clustering subsequently facilitates an IAM-mediated unwrapping of the ruptured vacuole membranes from S. flexneri, enabling the naked bacterium to be ready for intercellular spread via actin-based motility. Taken together, our work untangles the molecular cascade of S. flexneri-driven host trafficking subversion at IAMs to develop its cytosolic lifestyle, a crucial step en route for infection progression at cellular and tissue level.

Indexed as

Dysentery, BacillaryShigella flexneriSignal TransductionVacuolesBacterial ProteinsHeLa CellsHumansrab11 GTP-Binding Proteinsrab GTP-Binding ProteinsVirulence FactorsBacterial Proteinsrab11 GTP-Binding ProteinsRAB8A protein, humanrab GTP-Binding ProteinsVirulence Factors

Identifiers

PMID32866204
PMCPMC7485983
OpenAlexW3081543677

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.