Acaricidal Mechanism of Scopoletin Against Tetranychus cinnabarinus

Scopoletin is a promising acaricidal botanical natural compound against , and its acaricidal mechanism maybe involve calcium overload according to our previous study. To seek potential candidate target genes of calcium overload induced by scopoletin in , RNA-seq was utilized to detect changes in tra...

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Bibliographic Details
Published in:Frontiers in physiology 2019-03, Vol.10, p.164-164
Main Authors: Zhou, Hong, Zhang, Yong-Qiang, Lai, Ting, Liu, Xue-Jiao, Guo, Fu-You, Guo, Tao, Ding, Wei
Format: Article
Language:English
Subjects:
BAG
Ca2+ homeostasis
GPCR
GUK
Physiology
scopoletin
Tetranychus cinnabarinus
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Summary:Scopoletin is a promising acaricidal botanical natural compound against , and its acaricidal mechanism maybe involve calcium overload according to our previous study. To seek potential candidate target genes of calcium overload induced by scopoletin in , RNA-seq was utilized to detect changes in transcription levels. 24 and 48 h after treatment, 70 and 102 differentially expressed genes were obtained, respectively. Target genes included 3 signal transduction genes, 4 cell apoptosis genes, 4 energy metabolism genes, and 2 transcription factor genes. The role of 3 calcium signaling pathway-related genes, namely, G-protein-coupled neuropeptide receptor, Bcl-2 protein and guanylate kinase (designated , , and , respectively) in the calcium overload were investigated in this study. RT-qPCR detection showed that scopoletin treatment upregulated the expression level of and downregulated the expression level of and . The result of RNAi indicated that downregulation of decreased susceptibility to scopoletin, and downregulation of and enhanced susceptibility to scopoletin. Functional expression in Chinese hamster ovary cells showed that scopoletin induced a significant increase in intracellular free calcium [Ca ]i levels by activating These results demonstrated that the acaricidal mechanism of scopoletin was via disrupting intracellular Ca homeostasis and calcium signaling pathway mediated by GPCR, BAG, and GUK.
ISSN:1664-042X
1664-042X
DOI:10.3389/fphys.2019.00164