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家蚕蛹草拟青霉 microRNA-34-5p 通过靶向 odv-e66、ac78 和 ie2 调控杆状病毒的复制和感染

microRNA-34-5p encoded by Spodoptera frugiperda regulates the replication and infection of Autographa californica multiple nucleopolyhedrovirus by targeting odv-e66, ac78 and ie2.

机构信息

Key Laboratory of Chemical Biology and Molecular Engineering of Ministry of Education, Institute of Biotechnology, Shanxi University, Taiyuan, People's Republic of China.

Department of Medical Laboratory Science, Fenyang College, Shanxi Medical University, Fenyang, People's Republic of China.

出版信息

Pest Manag Sci. 2022 Dec;78(12):5379-5389. doi: 10.1002/ps.7160. Epub 2022 Sep 21.

Abstract

BACKGROUND

Spodoptera frugiperda is one of the significant migratory pests in the Global Alert issued by the Food and Agriculture Organization of the United Nations. As an insect-specific microbial insecticide, baculovirus has been used to control various pests. MicroRNA-34-5p (miR-34-5p) is involved in regulating growth, reproduction and innate immunity to pathogens in insects, playing an essential role in host-virus interactions. In this study, we explored the critical function of miR-34-5p encoded by S. frugiperda in the anti-Autographa californica multiple nucleopolyhedrovirus (AcMNPV), providing a reference for the design of a miR-34-5p target biopesticide against S. frugiperda and a theoretical basis for the wide application of microRNAs (miRNAs) in green pest control technology.

RESULTS

We focused on miR-34-5p identified as downregulated in Sf9 cells and S. frugiperda larvae infected by AcMNPV. The regulatory function of miR-34-5p in AcMNPV-S. frugiperda interactions was studied by transfecting synthetic mimics and inhibitors, and constructing recombinant bacmids with miR-34-5p overexpression. miR-34-5p inhibited the production of infectious budded virions at the cellular and insect levels, inhibited the replication of the viral DNA and glucose metabolism, and increased the transcription of the antimicrobial peptide gloverin. Furthermore, the virus genes odv-e66, ac78 and ie2 were shown to be direct targets.

CONCLUSION

We systematically revealed the mechanism by which miR-34-5p is involved in the insect antiviral process. miR-34-5p inhibited the replication and infection of AcMNPV by directly targeting AcMNPV genes, especially ac78 and ie2. Our study provides a new direction and thinking for the prevention and green control of lepidopteran pests. © 2022 Society of Chemical Industry.

摘要

背景

草地贪夜蛾是联合国粮食及农业组织全球预警的重大迁飞性害虫之一。杆状病毒作为昆虫特异性微生物杀虫剂,已被用于防治多种害虫。微小 RNA-34-5p(miR-34-5p)参与调控昆虫的生长、繁殖和对病原体的先天免疫,在宿主-病毒相互作用中发挥重要作用。本研究探讨了 S. frugiperda 编码的 miR-34-5p 在抗 AcMNPV 中的关键功能,为设计针对 S. frugiperda 的 miR-34-5p 靶标生物农药提供了参考,为 microRNAs(miRNAs)在绿色害虫防治技术中的广泛应用提供了理论依据。

结果

我们专注于 Sf9 细胞和感染 AcMNPV 的 S. frugiperda 幼虫中下调的 miR-34-5p。通过转染合成模拟物和抑制剂以及构建 miR-34-5p 过表达的重组 bacmids,研究了 miR-34-5p 在 AcMNPV-S. frugiperda 相互作用中的调控功能。miR-34-5p 在细胞和昆虫水平上抑制传染性芽生病毒粒子的产生,抑制病毒 DNA 的复制和葡萄糖代谢,并增加抗菌肽 gloverin 的转录。此外,还显示病毒基因 odv-e66、ac78 和 ie2 是直接靶标。

结论

我们系统地揭示了 miR-34-5p 参与昆虫抗病毒过程的机制。miR-34-5p 通过直接靶向 AcMNPV 基因,特别是 ac78 和 ie2,抑制 AcMNPV 的复制和感染。我们的研究为鳞翅目害虫的防治和绿色防治提供了新的方向和思路。© 2022 化学工业协会。

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