Insecticide resistance threatens effective pest management. In this study on Rhopalosiphum padi, a predominant wheat pest, a field-derived beta-cypermethrin-resistant strain (Beta-R strain) showed a 4623.50-fold resistance increase after 22 generations of beta-cypermethrin exposure and remained highly resistant (>4000-fold) after 40 generations without exposure. Beta-R strain exhibited a relative fitness of 0.92, high cross-resistance to lambda-cyhalothrin and bifenthrin, low-to-moderate resistance to sulfoxaflor, thiamethoxam, and imidacloprid, and negative or no resistance to omethoate and chlorpyrifos. The cytochrome P450 monooxygenases (P450s) and glutathione S-transferases (GSTs) contribute to this resistance. A homozygous spuer-kdr M918L mutation was identified in the IIS4–S6 region of the voltage-gated sodium channel gene in the Beta-R strain; however, transgenic Drosophila melanogaster assays showed that this mutation alone conferred only a 2.96-fold increase in beta-cypermethrin resistance. These findings show that resistant of R. padi to beta-cypermethrin can be retain high-level resistance without insecticide exposure, while also conferring high-level cross-resistance to other pyrethroids and low or negative resistance to other insecticides with different modes of action, with the resistance phenotype linked to upregulated P450/GST activities and an M918L mutation that makes only a minor contribution. These findings have significant implications for the management of resistance to pyrethroid insecticides in R. padi.
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Li et al. (2026) studied this question.
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