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CRISPR/Cas9-mediated knockout of CsRDL1 decreases the susceptibility of Chilo suppressalis to cyproflanilide.

Created on 05 Sep 2026

Authors

Jungang Zhou, Ziren Zang, Hongshuai Gao, Jinjun Sun, Lina Xu, Qiao Gao, Hualiang He, Wenbing Ding, Lin Qiu, Youzhi Li

Published in

Pesticide biochemistry and physiology. Volume 223. Pages 107282. Epub Jul 28, 2026.

Abstract

The novel meta-diamide insecticide cyproflanilide represents a promising tool for pest control, yet its precise molecular target remains uncharacterized. The RDL1 encodes a subunit of insect ionotropic GABA receptors (GABAr), which is targeted by meta-diamide pesticides. This study investigated the functional role of the resistance to dieldrin 1 (RDL1) subunit in Chilo suppressalis, a major rice pest, by generating a homozygous CsRDL1 knockout strain (CsRDL1-/-, lacking 101 bp) via CRISPR/Cas9-mediated gene editing. Bioassay results showed that the CsRDL1-/- strain exhibited a 2.67-fold increase in tolerance to cyproflanilide and a 3.08-fold increase to broflanilide, whereas its susceptibility to abamectin and emamectin benzoate, which also act on the CsRDL1 subunit, remained unchanged. These results indicate that knockout of CsRDL1 decreased susceptibility to cyproflanilide and broflanilide, and that the mode of action of these meta-diamides differs from that of abamectin and emamectin benzoate. Meanwhile, the CsRDL1-/- strain exhibited significant changes in key biological traits: 3rd-6th instar larval duration shortened by 9.45%, fecundity (eggs per female) reduced by 29.49%, and both pupal duration and female adult longevity were significantly shortened relative to the wild-type population. These findings provide in vivo evidence that CsRDL1 contributes to cyproflanilide susceptibility and plays important roles in development and reproduction in C. suppressalis. This study lays a foundation for further mechanistic studies on the interaction between cyproflanilide and CsRDL1 subunit, and offers insights for the development of insecticides targeting this subunit.

PMID:
42697651
Bibliographic data and abstract were imported from PubMed on 05 Sep 2026.

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