ArticleCommunications biology2023
A glutamate-gated chloride channel as the mite-specific target-site of dicofol and other diphenylcarbinol acaricides.
Article in Communications biology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 11 citations in OpenAlex.
- A complete genome sequence enables efficient genetic mapping of adaptive traits in a phytoseiid predatory mite (Amblyseius andersoni).Communications biology · 2026Article
- Exploring the efficacy of new potential bio-insecticides produced by Penicillium oxalicum against Culex pipiens larvae.BMC microbiology · 2026Article
- Population genomics reveal multiple independent origins of pesticide resistance in the polyphagous pest, Tetranychus urticae.Communications biology · 2025Article
- Bioinformatics Analysis of the Glutamate-Gated Chloride Channel Family inInternational journal of molecular sciences · 2025Article
- A glutamate-gated chloride channel as the mite-specific target-site of dicofol and other diphenylcarbinol acaricides.Communications biology · 2023Article
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Authors and funding
9 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Dicofol has been widely used to control phytophagous mites. Although dicofol is chemically related to DDT, its mode of action has remained elusive. Here, we mapped dicofol resistance in the spider mite Tetranychus urticae to two genomic regions. Each region harbored a glutamate-gated chloride channel (GluCl) gene that contained a mutation-G314D or G326E-known to confer resistance against the unrelated acaricide abamectin. Using electrophysiology assays we showed that dicofol and other diphenylcarbinol acaricides-bromopropylate and chlorobenzilate-induce persistent currents in Xenopus oocytes expressing wild-type T. urticae GluCl3 receptors and potentiate glutamate responses. In contrast, the G326E substitution abolished the agonistic activity of all three compounds. Assays with the wild-type Drosophila GluClα revealed that this receptor was unresponsive to dicofol. Homology modeling combined with ligand-docking confirmed the specificity of electrophysiology assays. Altogether, this work elucidates the mode of action of diphenylcarbinols as mite-specific agonists of GluCl.
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