Actin Assembly around the Shigella-Containing Vacuole Promotes Successful Infection.

Arp2/3 complex CDC42 N(ε) fatty acylation N-WASP Shigella flexneri actin cytoskeleton effector proteins host-pathogen interactions intracellular pathogens vacuolar rupture

Journal

Cell reports
ISSN: 2211-1247
Titre abrégé: Cell Rep
Pays: United States
ID NLM: 101573691

Informations de publication

Date de publication:
12 05 2020
Historique:
received: 30 09 2019
revised: 10 03 2020
accepted: 21 04 2020
entrez: 14 5 2020
pubmed: 14 5 2020
medline: 21 5 2021
Statut: ppublish

Résumé

The enteroinvasive bacterium Shigella flexneri forces its uptake into non-phagocytic host cells through the translocation of T3SS effectors that subvert the actin cytoskeleton. Here, we report de novo actin polymerization after cellular entry around the bacterium-containing vacuole (BCV) leading to the formation of a dynamic actin cocoon. This cocoon is thicker than any described cellular actin structure and functions as a gatekeeper for the cytosolic access of the pathogen. Host CDC42, TOCA-1, N-WASP, WIP, the Arp2/3 complex, cortactin, coronin, and cofilin are recruited to the actin cocoon. They are subverted by T3SS effectors, such as IpgD, IpgB1, and IcsB. IcsB immobilizes components of the actin polymerization machinery at the BCV dependent on its fatty acyltransferase activity. This represents a unique microbial subversion strategy through localized entrapment of host actin regulators causing massive actin assembly. We propose that the cocoon promotes subsequent invasion steps for successful Shigella infection.

Identifiants

pubmed: 32402280
pii: S2211-1247(20)30591-X
doi: 10.1016/j.celrep.2020.107638
pmc: PMC7225751
pii:
doi:

Substances chimiques

Actins 0

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

107638

Informations de copyright

Copyright © 2020 The Authors. Published by Elsevier Inc. All rights reserved.

Déclaration de conflit d'intérêts

Declaration of Interests The authors declare no competing interests.

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Auteurs

Sonja Kühn (S)

Institut Pasteur, Department of Cell Biology and Infection, Dynamics of Host-Pathogen Interactions Unit, 25 Rue du Dr. Roux, 75015 Paris, France; CNRS UMR3691, 25 Rue du Dr. Roux, 75015 Paris, France.

John Bergqvist (J)

Institut Pasteur, Department of Cell Biology and Infection, Dynamics of Host-Pathogen Interactions Unit, 25 Rue du Dr. Roux, 75015 Paris, France; CNRS UMR3691, 25 Rue du Dr. Roux, 75015 Paris, France.

Magdalena Gil (M)

Institut Pasteur, Department of Cell Biology and Infection, Dynamics of Host-Pathogen Interactions Unit, 25 Rue du Dr. Roux, 75015 Paris, France; CNRS UMR3691, 25 Rue du Dr. Roux, 75015 Paris, France.

Camila Valenzuela (C)

Institut Pasteur, Department of Cell Biology and Infection, Dynamics of Host-Pathogen Interactions Unit, 25 Rue du Dr. Roux, 75015 Paris, France; CNRS UMR3691, 25 Rue du Dr. Roux, 75015 Paris, France.

Laura Barrio (L)

Institut Pasteur, Department of Cell Biology and Infection, Dynamics of Host-Pathogen Interactions Unit, 25 Rue du Dr. Roux, 75015 Paris, France; CNRS UMR3691, 25 Rue du Dr. Roux, 75015 Paris, France.

Stéphanie Lebreton (S)

Institut Pasteur, Department of Cell Biology and Infection, Membrane Trafficking and Pathogenesis Unit, 28 Rue du Dr. Roux, 75015 Paris, France.

Chiara Zurzolo (C)

Institut Pasteur, Department of Cell Biology and Infection, Membrane Trafficking and Pathogenesis Unit, 28 Rue du Dr. Roux, 75015 Paris, France.

Jost Enninga (J)

Institut Pasteur, Department of Cell Biology and Infection, Dynamics of Host-Pathogen Interactions Unit, 25 Rue du Dr. Roux, 75015 Paris, France; CNRS UMR3691, 25 Rue du Dr. Roux, 75015 Paris, France. Electronic address: jost.enninga@pasteur.fr.

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