CDC25B promotes influenza A virus replication by regulating the phosphorylation of nucleoprotein.

CDC25B promotes influenza A virus replication by regulating the phosphorylation of nucleoprotein.
Virology. 2018 Sep 18;525:40-47
Authors: Cui L, Mahesutihan M, Zheng W, Meng L, Fan W, Li J, Ye X, Liu W, Sun L
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.
PMID: 30240957 [PubMed - as supplied by publisher]

Source: Virology - September 18, 2018 Category: Virology Authors: Cui L, Mahesutihan M, Zheng W, Meng L, Fan W, Li J, Ye X, Liu W, Sun L Tags: Virology Source Type: research