An autophagy-independent role for LC3 in equine arteritis virus replication

Autor: Iryna Monastyrska, Peter J. M. Rottier, Fulvio Reggiori, Mustafa Ulasli, Cornelis A. M. de Haan, Jun-Lin Guan
Rok vydání: 2013
Předmět:
autophagy
Diergeneeskunde
Viral Proteins/metabolism
Green Fluorescent Proteins
Virus Replication/physiology
Virus Replication
medicine.disease_cause
Virus
RNA Transport
Cell Line
Arterivirus
Geneeskunde
Viral Proteins
Mice
Equartevirus/physiology
Equartevirus
arterivirus
medicine
LC3
Autophagy
Animals
Arterivirus Infections/metabolism
Transport Vesicles
Molecular Biology
RNA
Double-Stranded

Coronavirus
Green Fluorescent Proteins/metabolism
Arterivirus Infections
biology
Cell Membrane/metabolism
Cell Membrane
Membrane Proteins
RNA
RNA virus
Cell Biology
biology.organism_classification
Virology
Basic Research Paper
Viral replication
Cell culture
Microtubule-Associated Proteins/metabolism
Transport Vesicles/metabolism
Membrane Proteins/metabolism
RNA
Double-Stranded/metabolism

double-membrane vesicles
Microtubule-Associated Proteins
nidoviruses
Zdroj: Autophagy
Monastyrska, I, Ulasli, M, Rottier, P J M, Guan, J-L, Reggiori, F & de Haan, C A M 2013, ' An autophagy-independent role for LC3 in equine arteritis virus replication ', Autophagy, vol. 9, no. 2, pp. 164-74 . https://doi.org/10.4161/auto.22743
Autophagy, 9(2), 1. Landes Bioscience
ISSN: 1554-8635
1554-8627
DOI: 10.4161/auto.22743
Popis: Equine arteritis virus (EAV) is an enveloped, positive-strand RNA virus. Genome replication of EAV has been associated with modified intracellular membranes that are shaped into double-membrane vesicles (DMVs). We showed by immuno-electron microscopy that the DMVs induced in EAV-infected cells contain double-strand (ds)RNA molecules, presumed RNA replication intermediates, and are decorated with the autophagy marker protein microtubule-associated protein 1 light chain 3 (LC3). Replication of EAV, however, was not affected in autophagy-deficient cells lacking autophagy-related protein 7 (ATG7). Nevertheless, colocalization of DMVs and LC3 was still observed in these knockout cells, which only contain the nonlipidated form of LC3. Although autophagy is not required, depletion of LC3 markedly reduced the replication of EAV. EAV replication could be fully restored in these cells by expression of a nonlipidated form of LC3. These findings demonstrate an autophagy-independent role for LC3 in EAV replication. Together with the observation that EAV-induced DMVs are also positive for ER degradation-enhancing α-mannosidase-like 1 (EDEM1), our data suggested that this virus, similarly to the distantly-related mouse hepatitis coronavirus, hijacks the ER-derived membranes of EDEMosomes to ensure its efficient replication.
Databáze: OpenAIRE