A glutamate-gated chloride channel as the mite-specific target-site of dicofol and other diphenylcarbinol acaricides

Marilou Vandenhole, Catherine Mermans, Berdien De Beer, Wenxin Xue, Yilan Zhao, Yoshihisa Ozoe, Genyan Liu, Wannes Dermauw, Thomas Van Leeuwen

Research output: Contribution to journalArticlepeer-review

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.

Original languageEnglish
Article number1160
JournalCommunications biology
Volume6
Issue number1
ISSN2399-3642
DOIs
Publication statusPublished - 13-Nov-2023

Keywords

  • Acaricides/pharmacology
  • Dicofol
  • Chloride Channels/genetics
  • Mutation

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