Molecular Characterization of Two Mitogen-Activated Protein Kinases: p38 MAP Kinase and Ribosomal S6 Kinase From Bombyx mori (Lepidoptera: Bombycidae), and Insight Into Their Roles in Response to BmNPV Infection

Muhammad, Azharuddin; Toufeeq, Shahzad; Yu, Hai-Zhong; Wang, Jie; Zhang, Shang-Zhi; Li, Bing; Li, Zhen; Yang, Li-Ang; Hu, Pei; Ma, Yan; Xu, Jia-Ping

For further confirmation of Bmp38 and BmS6K role in silkworm against BmNPV infection, we used BC9 (resistant strain) and blocked the proteins with corresponding antibodies. The results indicated that Bmp38 blocking increased the relative copy numbers of viral genes when compared with control. It has been reported that silence of p38 from Chinese shrimp (Fenneropenaeus chinensis) revealed its role against white spot syndrome virus (He et al. 2018) . Pharmacological inhibition of p38 MAPK by SB203580 affected the replication of influenza virus and respiratory syncytial virus (Marchant et al. 2010) . Therefore, we speculated that Bmp38 might be involved in BmNPV resistance. The RSK family comprised a group of highly related serine/threonine kinases that regulated diverse cellular processes, including proliferation, cell growth, and motility. Members of RSK family contained RSK1, RSK2, RSK3, and RSK4. Among them, activated RSK2 was shown to phosphorylate several transcription factors response to viral infection (Yan et al. 2018) . Surviladze et al. (2013) revealed that activation of PI3K/Akt/ mTOR could phosphorylate S6K to further activate the downstream signal pathways in response to human papillomavirus type 16 infection. In case of BmS6K, the relative copy numbers of viral genes were significantly upregulated than CK. We considered that BmNPV resistance of BmS6K required phosphorylation modification. Therefore, the specific reasons need to be conducted. The abovementioned results suggested that blocking of Bmp38 and BmS6K in BC9 (resistant strain) might participate in BmNPV proliferation.