Contrasting roles of cytochrome P450s in amitraz and chlorfenapyr resistance in the crop pest Tetranychus urticae

• Published in: Insect biochemistry and molecular biology Vol. 164; p. 104039
• Main Authors: Vandenhole, Marilou, Lu, Xueping, Tsakireli, Dimitra, Mermans, Catherine, De Rouck, Sander, De Beer, Berdien, Simma, Eba, Pergantis, Spiros A, Jonckheere, Wim, Vontas, John, Van Leeuwen, Thomas
• Format: Journal Article
• Language: English
• Published: England 01.01.2024
• Subjects: Acaricides - metabolism; Acaricides - pharmacology; Animals; Cytochrome P-450 Enzyme System - genetics; Cytochrome P-450 Enzyme System - metabolism; Humans; Pyrethrins - metabolism; Pyrethrins - pharmacology; Tetranychidae - genetics; Tetranychidae - metabolism; Toluidines - metabolism; Toluidines - pharmacology; Genetic mapping; Acaricide resistance; Gene regulation; Detoxification; Octopamine receptor; Spider mite; Mitochondrial uncouplers
• ISSN: 0965-1748; 1879-0240
• DOI: 10.1016/j.ibmb.2023.104039

The molecular mechanisms of amitraz and chlorfenapyr resistance remain only poorly understood for major agricultural pests and vectors of human diseases. This study focusses on a multi-resistant field strain of the crop pest Tetranychus urticae, which could be readily selected in the laboratory to high levels of amitraz and chlorfenapyr resistance. Toxicity experiments using tralopyril, the active toxophore of chlorfenapyr, suggested decreased activation as a likely mechanism underlying resistance. Starting from the same parental strain, transcriptome profiling revealed that a cluster of detoxifying genes was upregulated after amitraz selection, but unexpectedly downregulated after chlorfenapyr selection. Further functional validation associated the upregulation of CYP392A16 with amitraz metabolism and the downregulation of CYP392D8 with reduced activation of chlorfenapyr to tralopyril. Genetic mapping (QTL analysis by BSA) was conducted in an attempt to unravel the genetic mechanisms of expression variation and resistance. This revealed that chlorfenapyr resistance was associated with a single QTL, while 3 QTLs were uncovered for amitraz resistance. Together with the observed contrasting gene expression patterns, we argue that transcriptional regulators most likely underly the distinct expression profiles associated with resistance, but these await further functional validation.