Wang Chen, Guo Xiaojun, Li Yingqi, Zhang Jianzhen, Fu Yuejun
Key Laboratory of Chemical Biology and Molecular Engineering of Ministry of Education, Institute of Biotechnology, Shanxi University, Taiyuan 030006, China.
Institute of Quality Standard and Testing Technology, Beijing Academy of Agricultural and Forestry Science, Beijing 100097, China.
Int J Biol Macromol. 2022 Dec 1;222(Pt B):2190-2199. doi: 10.1016/j.ijbiomac.2022.09.293. Epub 2022 Oct 6.
Spodoptera frugiperda is one of the significant migratory pests. Baculovirus, an insect-specific microbial insecticide, has been used to control pests. microRNA-34 (miR-34) regulates insect development and innate immunity to pathogens. This study explored the critical functions of miR-34-5p, encoded by S. frugiperda, in the anti-AcMNPV by targeting the JAK/STAT immune pathway. Integrating immune signal pathways analysis, developmental expression patterns, larval development, and genomic replication assay, we focused on the stat, a miR-34-5p target gene, and comprehensively revealed a novel mechanism of physiological and anti-virus function in S. frugiperda. miR-34-5p inhibited AcMNPV proliferation by targeting stat and provided an unfavorable environment for the virus by affecting the host genome replication and promoting the cell to undergo apoptosis. Moreover, stat silence suppressed viral and host genome replication, impaired viral proliferation by suppressing the transcript level of viral early gene ie1, ie2, and promoted apoptosis by affecting p35 expression. This study highlighted that the miR-34-5p target gene stat played physiological functions in the insect antiviral immune and development, which provided a basis for creating target nucleic acid pesticides against S. frugiperda and prepared AcMNPV virus strains inactivated by miR-34-5p to escape host immunity.
草地贪夜蛾是重要的迁飞性害虫之一。杆状病毒是一种昆虫特异性微生物杀虫剂,已被用于防治害虫。微小RNA-34(miR-34)调节昆虫发育和对病原体的先天免疫。本研究通过靶向JAK/STAT免疫途径,探讨了草地贪夜蛾编码的miR-34-5p在抗苜蓿银纹夜蛾核型多角体病毒(AcMNPV)中的关键作用。结合免疫信号通路分析、发育表达模式、幼虫发育和基因组复制分析,我们聚焦于miR-34-5p的靶基因stat,全面揭示了草地贪夜蛾生理和抗病毒功能的新机制。miR-34-5p通过靶向stat抑制AcMNPV增殖,并通过影响宿主基因组复制和促进细胞凋亡为病毒提供不利环境。此外,stat沉默抑制病毒和宿主基因组复制,通过抑制病毒早期基因ie1、ie2的转录水平损害病毒增殖,并通过影响p35表达促进细胞凋亡。本研究强调,miR-34-5p靶基因stat在昆虫抗病毒免疫和发育中发挥生理功能,为创制针对草地贪夜蛾的靶标核酸农药以及制备被miR-34-5p灭活以逃避宿主免疫的AcMNPV病毒株提供了依据。