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Published on: October 28, 2019
Mink enteritis virus infection induced cell cycle arrest and autophagy for its replication
Dong Lu-Jiao1, Li Zhi-Juan2, Sun Ying-Li1
1Shandong Provincial Key Laboratory of Zoonoses, Shandong Agricultural University, Taian, Shandong Province 271018, China; College of Veterinary Medicine, Shandong Agricultural University, Taian, Shandong Province 271018, China.
Abstract:
Mink enteritis virus (MEV) is an important pathogen causing mink viral enteritis. The mechanisms of cell cycle arrest induced by MEV infection and the roles of autophagy in MEV replication remain unclear. In this study, the roles of MEV NS1 protein in inducing cell cycle arrest were investigated, using the in vitro CRFK cell models. As a result, MEV infection increased the proportion of the cells in S phase, inducing S phase arrest. MEV NS1 protein also led to cycle arrest in S phase. And the deletions of NLS and TAD significantly weakened the ability of NS1 protein to cause cycle arrest in S phase, and NLS and TAD were the indispensable domains of NS1 protein. Furthermore, proteome profiling of the cells infected with MEV at the early stage demonstrated that the autophagy-related protein TRIM23 was significantly up-regulated during MEV infection. To investigate the effects of TRIM23 on MEV replication, the cell models were established, using siRNAs targeting TRIM23. The knockdown of TRIM23 resulted in the decreases in the levels of TBK1 protein and the phosphorylated p62 protein, and an increase in the level of p62 protein in the cells infected with MEV, indirectly influencing virus replication. The findings implied that S phase arrest and the up-regulated TRIM23 induced by MEV infection played the important roles in MEV replication.
Insights
Mink enteritis virus (MEV) causes S phase arrest via its NS1 protein, impacting viral replication. Upregulated TRIM23 protein also plays a role in MEV infection.
Area of Science:
- Virology
- Cell Biology
- Molecular Biology
Background:
- Mink enteritis virus (MEV) causes significant disease in mink.
- The precise mechanisms of MEV-induced cell cycle arrest and the involvement of autophagy in MEV replication are not fully understood.
Purpose of the Study:
- To investigate the role of MEV NS1 protein in inducing cell cycle arrest.
- To explore the function of autophagy-related protein TRIM23 in MEV replication.
Main Methods:
- In vitro CRFK cell models were used to study MEV infection.
- MEV NS1 protein domains (NLS and TAD) were analyzed for their role in cell cycle arrest.
- Proteome profiling identified TRIM23 upregulation during MEV infection.
- siRNA-mediated knockdown of TRIM23 was performed to assess its impact on MEV replication.
Main Results:
- MEV infection and NS1 protein induced S phase arrest in CRFK cells.
- The NLS and TAD domains of NS1 protein were essential for inducing S phase arrest.
- MEV infection led to significant upregulation of the autophagy-related protein TRIM23.
- TRIM23 knockdown affected TBK1 and p62 protein levels, indirectly influencing MEV replication.
Conclusions:
- MEV infection induces S phase arrest, partly mediated by the NS1 protein's NLS and TAD domains.
- Upregulation of TRIM23 is a significant host response to MEV infection and influences viral replication.
- Both S phase arrest and TRIM23 play crucial roles in the replication of mink enteritis virus.
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