Abstract
Scopoletin is a promising acaricidal botanical natural compound against Tetranychus cinnabarinus, 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 T. cinnabarinus, 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 TcGPCR, TcBAG, and TcGUK, respectively) in the calcium overload were investigated in this study. RT-qPCR detection showed that scopoletin treatment upregulated the expression level of TcGPCR and downregulated the expression level of TcBAG and TcGUK. The result of RNAi indicated that downregulation of TcGPCR decreased susceptibility to scopoletin, and downregulation of TcBAG and TcGUK enhanced susceptibility to scopoletin. Functional expression in Chinese hamster ovary cells showed that scopoletin induced a significant increase in intracellular free calcium [Ca2+]i levels by activating TcGPCR. These results demonstrated that the acaricidal mechanism of scopoletin was via disrupting intracellular Ca2+ homeostasis and calcium signaling pathway mediated by GPCR, BAG, and GUK.
Highlights
The carmine spider mite, Tetranychus cinnabarinus, is one of the most polyphagous arthropod herbivores and feeds on more than 100 plant species, such as food and economic crops, ornamental plants, and weeds (Zhang et al, 2004; Çakmak et al, 2005; Sarwar, 2013)
Functional expression in Chinese hamster ovary cells showed that scopoletin induced a significant increase in intracellular free calcium [Ca2+]i levels by activating TcGPCR. These results demonstrated that the acaricidal mechanism of scopoletin was via disrupting intracellular Ca2+ homeostasis and calcium signaling pathway mediated by GPCR, BAG, and GUK
We found that a significant increase in intracellular calcium level in insect Sf9 cells was induced by scopoletin in a concentration-dependent manner, indicating that the mode of action of scopoletin in insects was by inducing intracellular calcium overload
Summary
The carmine spider mite, Tetranychus cinnabarinus, is one of the most polyphagous arthropod herbivores and feeds on more than 100 plant species, such as food and economic crops, ornamental plants, and weeds (Zhang et al, 2004; Çakmak et al, 2005; Sarwar, 2013). The carmine spider mite is parthenogenic and exhibits strong adaptability and fecundity. This type of mite is one of the most difficult pests to control because it develops resistance to pesticides (Cruz et al, 2013). A previous study found that scopoletin exhibits excellent contact killing, as well as systemic, repellent, and oviposition inhibition activities against T. cinnabarinus (Zhou et al, 2017). Mites did not develop resistance against scopoletin after 18 generations possibly because of the multi-target mechanism of scopoletin against T. cinnabarinus (Zhang et al, 2011). After exposure to scopoletin, several typical neurotoxic symptoms, such as excitement and convulsions, were observed in mites, and the compound inhibits the nervous system targets, AChE, Na+-K+-ATPase, Ca2+-Mg2+-ATPase, and Ca2+-ATPase, which indicates that scopoletin is a neurotoxin, in which Ca2+ plays a key role as an intracellular second messenger (Liang et al, 2011; Hou et al, 2015)
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
