Wei Lili, Liang Aihua, Fu Yuejun
Key Laboratory of Chemical Biology and Molecular Engineering of Ministry of Education, Institute of Biotechnology, Shanxi University Taiyuan 030006 China
RSC Adv. 2018 Sep 4;8(54):31071-31080. doi: 10.1039/c8ra05172k. eCollection 2018 Aug 30.
Baculovirus encoded PK2 protein can increase viral fitness through inhibition of the eIF2α family kinases activity. Previous studies indicated that the virus might take over the control of cellular machinery post-infection, which would impose a high metabolic burden to infected insect cells. Here we showed that eIF2α phosphorylation decreased, with concomitant up-regulation of total and heterologous protein synthesis in AcMNPV-PK2-EGFP infected Sf9 cells and the larvae of . Simultaneously, the lactic acid accumulation decreased and the uptake of glucose increased in AcMNPV-PK2-EGFP infected Sf9 cells. We proposed a model that Ac-PK2 protein overexpression would help protein synthesis by inhibiting eIF2α phosphorylation, which provided a more favorable scenario to support the efficient replication of the virus by re-directing the cellular metabolism toward ATP production. Finally, we confirmed that AcMNPV-PK2-EGFP could improve the production of progeny virus in infected Sf9 cells and enhance insecticidal activity against larvae.
杆状病毒编码的PK2蛋白可通过抑制eIF2α家族激酶的活性来提高病毒适应性。先前的研究表明,病毒在感染后可能会接管细胞机制的控制,这会给受感染的昆虫细胞带来很高的代谢负担。在这里,我们发现,在感染AcMNPV-PK2-EGFP的Sf9细胞和[具体昆虫名称缺失]幼虫中,eIF2α磷酸化水平降低,同时总蛋白和异源蛋白的合成上调。同时,感染AcMNPV-PK2-EGFP的Sf9细胞中乳酸积累减少,葡萄糖摄取增加。我们提出了一个模型,即Ac-PK2蛋白的过表达通过抑制eIF2α磷酸化来帮助蛋白质合成,这通过将细胞代谢重定向到ATP产生,为支持病毒的有效复制提供了更有利的条件。最后,我们证实AcMNPV-PK2-EGFP可以提高感染的Sf9细胞中后代病毒的产量,并增强对[具体昆虫名称缺失]幼虫的杀虫活性。