Porcine hemagglutinating encephalomyelitis virus induces atypical autophagy via opposite regulation of expression and nuclear translocation of transcription factor EB.
Active Transport, Cell Nucleus
Animals
Autophagy
/ physiology
Basic Helix-Loop-Helix Leucine Zipper Transcription Factors
/ genetics
Betacoronavirus 1
Cell Line
Gene Expression Regulation
Lysosomal Membrane Proteins
/ genetics
Mechanistic Target of Rapamycin Complex 1
/ genetics
Mice
Swine
Virus Replication
/ physiology
MTORC1 kinase
Opposite regulation
Porcine hemagglutinating encephalomyelitis virus
Transcription factor EB
Journal
Veterinary microbiology
ISSN: 1873-2542
Titre abrégé: Vet Microbiol
Pays: Netherlands
ID NLM: 7705469
Informations de publication
Date de publication:
Apr 2021
Apr 2021
Historique:
received:
18
10
2020
accepted:
14
02
2021
pubmed:
1
3
2021
medline:
21
9
2021
entrez:
28
2
2021
Statut:
ppublish
Résumé
Porcine hemagglutinating encephalomyelitis virus (PHEV) displays neurotropism and induces atypical autophagy. However, the exact mechanisms mediating autophagy induced by PHEV remains uncharacterized. Transcription factor EB (TFEB) is a master transcriptional regulator playing a key role in autophagy and its activity is regulated by MTORC1 kinase on the surface of lysosomes. We first found that PHEV infection decreases TFEB expression, while it activates TFEB by inhibiting MTORC1 activation, indicating that TFEB plays a complex role in the process of PHEV-induced autophagy through opposite regulation of its expression and activity. Furthermore, this study preliminarily demonstrated that PHEV replication is dependent on TFEB expression.
Identifiants
pubmed: 33640682
pii: S0378-1135(21)00038-9
doi: 10.1016/j.vetmic.2021.109015
pii:
doi:
Substances chimiques
Basic Helix-Loop-Helix Leucine Zipper Transcription Factors
0
Lamp1 protein, mouse
0
Lysosomal Membrane Proteins
0
Tcfeb protein, mouse
0
Mechanistic Target of Rapamycin Complex 1
EC 2.7.11.1
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
109015Informations de copyright
Copyright © 2021 Elsevier B.V. All rights reserved.