Abstract
Synergists can counteract metabolic insecticide resistance by inhibiting detoxification enzymes or transporters. They are used in commercial formulations of insecticides, but are also frequently used in the elucidation of resistance mechanisms. However, the effect of synergists on genome-wide transcription in arthropods is poorly understood. In this study we used Illumina RNA-sequencing to investigate genome-wide transcriptional responses in an acaricide resistant strain of the spider mite Tetranychus urticae upon exposure to synergists such as S,S,S-tributyl phosphorotrithioate (DEF), diethyl maleate (DEM), piperonyl butoxide (PBO) and cyclosporin A (CsA). Exposure to PBO and DEF resulted in a broad transcriptional response and about one third of the differentially expressed genes (DEGs), including cytochrome P450 monooxygenases and UDP-glycosyltransferases, was shared between both treatments, suggesting common transcriptional regulation. Moreover, both DEF and PBO induced genes that are strongly implicated in acaricide resistance in the respective strain. In contrast, CsA treatment mainly resulted in downregulation of Major Facilitator Superfamily (MFS) genes, while DEGs of the DEM treatment were not significantly enriched for any GO-terms.
Highlights
Insecticide resistance is a major threat for the agricultural productivity of commercial crops[1], and understanding the mechanisms underlying insecticide resistance is a high priority for the design and implementation of effective resistance management programs[2]
Human P-glycoproteins are well-known for their role in protecting tissues from toxic xenobiotics and endogenous metabolites[26] and in the last decade their counterparts in arthropods have been linked to insecticide transport and/or resistance[27,28]
piperonyl butoxide (PBO) has been reported to act as an inhibitor of esterases in Helicoverpa armigera, Frankliniella occidentalis and Bemisia tabaci[35,36,37] and as an inhibitor of mammalian UGTs38, while DEF was shown to act, albeit to a much lower extent compared to PBO, as an inhibitor of P450 monooxygenases (P450s) in Blatella germanica[34]
Summary
Insecticide resistance is a major threat for the agricultural productivity of commercial crops[1], and understanding the mechanisms underlying insecticide resistance is a high priority for the design and implementation of effective resistance management programs[2]. The inhibition mechanism of PBO consists of two phases, starting with the binding of PBO to the active site of the P450, followed by the formation of a quasi-irreversible inhibitor complex between the electrophilic carbene moiety of PBO and the ferrous iron of the P450 This results in a decreased metabolic activity of the P450 enzyme[7,14,15]. PBO has been reported to act as an inhibitor of esterases in Helicoverpa armigera, Frankliniella occidentalis and Bemisia tabaci[35,36,37] and as an inhibitor of mammalian UGTs38, while DEF was shown to act, albeit to a much lower extent compared to PBO, as an inhibitor of P450s in Blatella germanica[34] These studies suggest that in some cases caution should be applied in interpreting results of synergist application as they are not entirely specific to a single detoxification enzyme class[37,39,40]. Confirmation of P450 rather than esterase inhibition by PBO is straightforward and can be done with another class of P450 inhibitors[13]
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