Back to Search
Start Over
β-catenin facilitates fowl adenovirus serotype 4 replication through enhancing virus-induced autophagy.
- Source :
-
Veterinary Microbiology . Jan2023, Vol. 276, pN.PAG-N.PAG. 1p. - Publication Year :
- 2023
-
Abstract
- β-catenin is a key component of the Wnt/β-catenin signal transduction cascade which is a highly conserved signaling pathway in eukaryotes. Increasing evidence suggests that the Wnt/β-catenin signaling pathway is involved in the infection of many viruses. However, its role in fowl adenovirus serotype 4 (FAdV-4) replication remains unclear. In the present study, we showed that FAdV-4 infection increased the expression of β-catenin and promoted the nuclear translocation of β-catenin. Overexpression of β-catenin and LiCl treatment stimulated the accumulation of β-catenin in the nucleus, and then facilitated FAdV-4 replication. Conversely, repression of β-catenin by inhibitors and siRNA significantly inhibited FAdV-4 replication. Furthermore, inhibition of autophagy by 3-Methyladenine (3-MA) suppressed the FAdV-4 replication, and repression of β-catenin inhibited the FAdV-4-triggered autophagy. In conclusion, the nuclear translocation of β-catenin benefits FAdV-4 replication, and suppression of β-catenin limits FAdV-4 production by inhibiting FAdV-4-induced autophagy. These findings indicated that β-catenin is an important regulator of FAdV-4 replication which can serve as a potential target for anti-FAdV-4 agents. • FAdV-4 infection increases the expression of β-catenin and promotes the nuclear translocation of β-catenin. • The nuclear translocation of β-catenin facilitates FAdV-4 replication. • Suppression of β-catenin limits FAdV-4 production by inhibiting FAdV-4-induced autophagy. [ABSTRACT FROM AUTHOR]
- Subjects :
- *AUTOPHAGY
*POULTRY
*FOWLING
*CELLULAR signal transduction
*VIRUS diseases
Subjects
Details
- Language :
- English
- ISSN :
- 03781135
- Volume :
- 276
- Database :
- Academic Search Index
- Journal :
- Veterinary Microbiology
- Publication Type :
- Academic Journal
- Accession number :
- 160909591
- Full Text :
- https://doi.org/10.1016/j.vetmic.2022.109617