SrasV1, Main, Exploration, bibRecord, 002560

Coronaviruses Hijack the LC3-I-positive EDEMosomes, ER-derived vesicles exporting short-lived ERAD regulators, for replication.

Identifieur interne : 002560 ( Main/Exploration ); précédent : 002559; suivant : 002561

Coronaviruses Hijack the LC3-I-positive EDEMosomes, ER-derived vesicles exporting short-lived ERAD regulators, for replication.

Auteurs : Fulvio Reggiori [Pays-Bas] ; Iryna Monastyrska ; Monique H. Verheije ; Tito Calì ; Mustafa Ulasli ; Siro Bianchi ; Riccardo Bernasconi ; Cornelis A M. De Haan ; Maurizio Molinari

Source :

Cell host & microbe [ 1934-6069 ] ; 2010.

RBID : pubmed:20542253

Descripteurs français

KwdFr :
- Animaux, Cellules cultivées, Microscopie confocale, Microscopie de fluorescence, Microscopie électronique à transmission, Protéines associées aux microtubules (analyse), Protéines membranaires (métabolisme), Réplication virale, Réticulum endoplasmique (virologie), Ubiquitines (analyse), Virus de l'hépatite murine (physiologie), Vésicules cytoplasmiques (), Vésicules cytoplasmiques (virologie).
MESH :
- analyse : Protéines associées aux microtubules, Ubiquitines.
- métabolisme : Protéines membranaires.
- physiologie : Virus de l'hépatite murine.
- virologie : Réticulum endoplasmique, Vésicules cytoplasmiques.
- Animaux, Cellules cultivées, Microscopie confocale, Microscopie de fluorescence, Microscopie électronique à transmission, Réplication virale, Vésicules cytoplasmiques.

English descriptors

KwdEn :
- Animals, Cells, Cultured, Cytoplasmic Vesicles (chemistry), Cytoplasmic Vesicles (virology), Endoplasmic Reticulum (virology), Membrane Proteins (metabolism), Microscopy, Confocal, Microscopy, Electron, Transmission, Microscopy, Fluorescence, Microtubule-Associated Proteins (analysis), Murine hepatitis virus (physiology), Ubiquitins (analysis), Virus Replication.
MESH :
- chemical , analysis : Microtubule-Associated Proteins, Ubiquitins.
- chemical , metabolism : Membrane Proteins.
- chemistry : Cytoplasmic Vesicles.
- physiology : Murine hepatitis virus.
- virology : Cytoplasmic Vesicles, Endoplasmic Reticulum.
- Animals, Cells, Cultured, Microscopy, Confocal, Microscopy, Electron, Transmission, Microscopy, Fluorescence, Virus Replication.

Abstract

Coronaviruses (CoV), including SARS and mouse hepatitis virus (MHV), are enveloped RNA viruses that induce formation of double-membrane vesicles (DMVs) and target their replication and transcription complexes (RTCs) on the DMV-limiting membranes. The DMV biogenesis has been connected with the early secretory pathway. CoV-induced DMVs, however, lack conventional endoplasmic reticulum (ER) or Golgi protein markers, leaving their membrane origins in question. We show that MHV co-opts the host cell machinery for COPII-independent vesicular ER export of a short-living regulator of ER-associated degradation (ERAD), EDEM1, to derive cellular membranes for replication. MHV infection causes accumulation of EDEM1 and OS-9, another short-living ER chaperone, in the DMVs. DMVs are coated with the nonlipidated LC3/Atg8 autophagy marker. Downregulation of LC3, but not inactivation of host cell autophagy, protects cells from CoV infection. Our study identifies the host cellular pathway hijacked for supplying CoV replication membranes and describes an autophagy-independent role for nonlipidated LC3-I.

DOI: 10.1016/j.chom.2010.05.013
PubMed: 20542253

Affiliations:

Pays-Bas

Le document en format XML

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<term>Microscopy, Electron, Transmission</term>
<term>Microscopy, Fluorescence</term>
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<term>Microscopie électronique à transmission</term>
<term>Protéines associées aux microtubules (analyse)</term>
<term>Protéines membranaires (métabolisme)</term>
<term>Réplication virale</term>
<term>Réticulum endoplasmique (virologie)</term>
<term>Ubiquitines (analyse)</term>
<term>Virus de l'hépatite murine (physiologie)</term>
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<term>Vésicules cytoplasmiques (virologie)</term>
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<front><div type="abstract" xml:lang="en">Coronaviruses (CoV), including SARS and mouse hepatitis virus (MHV), are enveloped RNA viruses that induce formation of double-membrane vesicles (DMVs) and target their replication and transcription complexes (RTCs) on the DMV-limiting membranes. The DMV biogenesis has been connected with the early secretory pathway. CoV-induced DMVs, however, lack conventional endoplasmic reticulum (ER) or Golgi protein markers, leaving their membrane origins in question. We show that MHV co-opts the host cell machinery for COPII-independent vesicular ER export of a short-living regulator of ER-associated degradation (ERAD), EDEM1, to derive cellular membranes for replication. MHV infection causes accumulation of EDEM1 and OS-9, another short-living ER chaperone, in the DMVs. DMVs are coated with the nonlipidated LC3/Atg8 autophagy marker. Downregulation of LC3, but not inactivation of host cell autophagy, protects cells from CoV infection. Our study identifies the host cellular pathway hijacked for supplying CoV replication membranes and describes an autophagy-independent role for nonlipidated LC3-I.</div>
</front>
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<name sortKey="Cali, Tito" sort="Cali, Tito" uniqKey="Cali T" first="Tito" last="Calì">Tito Calì</name>
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Serveur d'exploration SRAS

Coronaviruses Hijack the LC3-I-positive EDEMosomes, ER-derived vesicles exporting short-lived ERAD regulators, for replication.

Coronaviruses Hijack the LC3-I-positive EDEMosomes, ER-derived vesicles exporting short-lived ERAD regulators, for replication.

Source :

Descripteurs français

English descriptors

Abstract

Links toward previous steps (curation, corpus...)

Le document en format XML

Pour manipuler ce document sous Unix (Dilib)

Pour mettre un lien sur cette page dans le réseau Wicri

Pour générer des pages wiki

	Serveur d'exploration SRAS
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