1. CDC25B promotes influenza A virus replication by regulating the phosphorylation of nucleoprotein.
- Author
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Cui, Liang, Mahesutihan, Madina, Zheng, Weinan, Meng, Lijun, Fan, Wenhui, Li, Jing, Ye, Xin, Liu, Wenjun, and Sun, Lei
- Subjects
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INFLUENZA A virus , *VIRAL replication , *PHOSPHORYLATION , *NUCLEOPROTEINS , *PROMOTERS (Genetics) , *CELL division - Abstract
Abstract Cell division cycle 25 B (CDC25B) is a member of the CDC25 phosphatase family. It can dephosphorylate cyclin-dependent kinases and regulate the cell division cycle. Moreover, siRNA knockdown of CDC25B impairs influenza A virus (IAV) replication. Here, to further understand the regulatory mechanism of CDC25B for IAV replication, a CDC25B-knockout (KO) 293T cell line was constructed using CRISPR/Cas9. The present data indicated that the replication of IAV was decreased in CDC25B-KO cells. Additionally, CDC25B deficiency damaged viral polymerase activity, nucleoprotein (NP) self-oligomerization, and NP nuclear export. Most importantly, we found that the NP phosphorylation levels were significantly increased in CDC25B-KO cells. These findings indicate that CDC25B facilitates the dephosphorylation of NP, which is vital for regulating NP functions and the life cycle of IAV. [ABSTRACT FROM AUTHOR]
- Published
- 2018
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