miR-34-5p, encoded by Spodoptera frugiperda, participates in anti-baculovirus by regulating innate immunity in the insect host
文献类型： 外文期刊
作者： Wang, Chen 1 ; Guo, Xiaojun 2 ; Li, Yingqi 3 ; Zhang, Jianzhen 4 ; Fu, Yuejun 1 ;
作者机构： 1.Shanxi Univ, Inst Biotechnol, Key Lab Chem Biol & Mol Engn, Minist Educ, Taiyuan 030006, Peoples R China
2.Beijing Acad Agr & Forestry Sci, Inst Qual Stand & Testing Technol, Beijing 100097, Peoples R China
3.Shanxi Univ, Sch Chem & Chem Engn, Taiyuan 030006, Peoples R China
4.Shanxi Univ, Inst Appl Biol, Taiyuan 030006, Peoples R China
关键词： Autographa californica multiple; nucleopolyhedrovirus (AcMNPV); microRNA-34-5p; Spodoptera frugiperda
期刊名称：INTERNATIONAL JOURNAL OF BIOLOGICAL MACROMOLECULES （ 影响因子：8.025； 五年影响因子：7.626 ）
ISSN： 0141-8130
年卷期： 2022 年 222 卷
页码：
收录情况： SCI
摘要： 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 antiAcMNPV 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 miR34-5p 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.
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