CDC25B promotes influenza A virus replication by regulating the phosphorylation of nucleoprotein
CDC25B promotes influenza A virus replication by regulating the phosphorylation of nucleoprotein
复制标题
CDC25B通过调节核蛋白磷酸化促进甲型流感病毒复制
DOI：
10.1016/j.virol.2018.09.005
复制
发表时间：
2018-12-01
期刊：
影响因子：
3.7
通讯作者：
Sun, Lei
中科院分区：
文献类型：
--
作者：
Cui, Liang;Mahesutihan, Madina;Sun, Lei
细胞分裂周期25b （CDC25B）是CDC25磷酸酶家族的一员。它可以使周期蛋白依赖性激酶去磷酸化并调节细胞分裂周期。此外，CDC25B的siRNA敲低会损害甲型流感病毒（IAV）的复制。为了进一步了解CDC25B对IAV复制的调控机制，我们利用CRISPR/Cas9技术构建了CDC25B敲除（KO） 293T细胞系。目前的数据表明，IAV在CDC25B-KO细胞中的复制减少。此外，CDC25B缺乏会破坏病毒聚合酶活性、核蛋白（NP）自寡聚和NP核输出。最重要的是，我们发现CDC25B-KO细胞的NP磷酸化水平显著升高。这些发现表明，CDC25B促进了NP的去磷酸化，这对于调节NP功能和LAV的生命周期至关重要。
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 LAV.