Legionella Manipulates Non-canonical SNARE Pairing Using a Bacterial Deubiquitinase.

COPI Legionella SNARE Sec22b deubiquitinase early secretory pathway effector protein syntaxin type IV secretion system ubiquitin

Journal

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

Informations de publication

Date de publication:
08 09 2020
Historique:
received: 19 10 2019
revised: 30 05 2020
accepted: 12 08 2020
entrez: 9 9 2020
pubmed: 10 9 2020
medline: 29 5 2021
Statut: ppublish

Résumé

The intracellular bacterial pathogen Legionella pneumophila uses many effector proteins delivered by the bacterial type IV secretion system (T4SS) to hijack the early secretory pathway to establish its replicative niche, known as the Legionella-containing vacuole (LCV). On LCV biogenesis, the endoplasmic reticulum (ER) vesicular soluble N-ethylmaleimide-sensitive factor attachment protein receptors (v-SNARE) Sec22b is recruited to the bacterial phagosome and forms non-canonical pairings with target membrane SNAREs (t-SNAREs) from the plasma membrane. Here, we identify a Legionella deubiquitinase (DUB), LotB, that can modulate the early secretory pathway by interacting with coatomer protein complex I (COPI) vesicles when ectopically expressed. We show that Sec22b is ubiquitinated upon L. pneumophila infection in a T4SS-dependent manner and that, subsequently, LotB deconjugates K63-linked ubiquitins from Sec22b. The DUB activity of LotB stimulates dissociation of the t-SNARE syntaxin 3 (Stx3) from Sec22b, which resides on the LCV. Our study highlights a bacterial strategy manipulating the dynamics of infection-induced SNARE pairing using a bacterial DUB.

Identifiants

pubmed: 32905772
pii: S2211-1247(20)31096-2
doi: 10.1016/j.celrep.2020.108107
pii:
doi:

Substances chimiques

Bacterial Proteins 0
Deubiquitinating Enzymes EC 3.4.19.12

Types de publication

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

Langues

eng

Sous-ensembles de citation

IM

Pagination

108107

Informations de copyright

Copyright © 2020 The Author(s). Published by Elsevier Inc. All rights reserved.

Déclaration de conflit d'intérêts

Declaration of Interests The authors declare no competing interests.

Auteurs

Tomoe Kitao (T)

Department of Microbiology, Graduate School of Medicine, Gifu University, Gifu, Gifu 501-1194, Japan.

Kyoichiro Taguchi (K)

Department of Microbiology, Graduate School of Medicine, Gifu University, Gifu, Gifu 501-1194, Japan; Laboratory of Veterinary Microbiology, Faculty of Applied Biological Science, Gifu University, Gifu, Gifu 501-1193, Japan.

Shintaro Seto (S)

Department of Pathophysiology and Host Defense, The Research Institute of Tuberculosis, Japan Anti-Tuberculosis Association, Kiyose, Tokyo 204-8533, Japan.

Kohei Arasaki (K)

School of Life Sciences, Tokyo University of Pharmacy and Life Sciences, Hachioji, Tokyo 192-0392, Japan.

Hiroki Ando (H)

G-CHAIN, Gifu University, Gifu, Gifu 501-1194, Japan; Laboratory of Phage Biologics, Graduate School of Medicine, Gifu University, Gifu, Gifu 501-1194, Japan.

Hiroki Nagai (H)

Department of Microbiology, Graduate School of Medicine, Gifu University, Gifu, Gifu 501-1194, Japan; G-CHAIN, Gifu University, Gifu, Gifu 501-1194, Japan. Electronic address: hnagai@gifu-u.ac.jp.

Tomoko Kubori (T)

Department of Microbiology, Graduate School of Medicine, Gifu University, Gifu, Gifu 501-1194, Japan; G-CHAIN, Gifu University, Gifu, Gifu 501-1194, Japan. Electronic address: tkubori@gifu-u.ac.jp.

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