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Research Progress on Chemical Control Status and Insecticide Resistance of Key Aphid Species
YANGHanjing, ZHAOJun, LIHang, ZHANGShuai
Chin Agric Sci Bull ›› 2026, Vol. 42 ›› Issue (12) : 186-198.
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Abbreviation (ISO4): Chin Agric Sci Bull
Editor in chief: Yulong YIN
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Research Progress on Chemical Control Status and Insecticide Resistance of Key Aphid Species
Aphids are major agricultural pests that infest a wide range of host species, causing substantial damage and economic losses to crops. This study was conducted to provide a reference for the prevention and control strategies and sustainable management of aphid populations. While chemical control remains a primary method for managing aphid populations, the rapid emergence of pesticide resistance poses a growing challenge. This study summarizes the globally prevalent and highly damaging aphid species, elaborating on their host ranges, distribution, and modes of infestation. It focuses on analyzing the current development of resistance to various insecticides, including organophosphates, pyrethroids, neonicotinoids, as well as sulfoxaflor and spirotetramat. Research indicates that aphids develop resistance through multiple mechanisms, such as reduced target-site sensitivity, decreased cuticular penetration, and enhanced metabolic enzyme activity, with the overexpression of cytochrome P450 genes and mutations in nAChR genes serving as the primary mechanisms. Based on current resistance trends, it is recommended that future efforts should strengthen the development of novel mode-of-action insecticides, deepen molecular-level research on resistance mechanisms, and formulate integrated management strategies centered on insecticide rotation and biological control, thereby providing theoretical and technical support for achieving green and sustainable aphid control.
aphid / damage / host plants / chemical control / resistance mechanism
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The frequent use of insecticides to manage soybean aphids, Aphis glycines (Hemiptera: Aphididae), in the United States has contributed to field-evolved resistance. Pyrethroid-resistant aphids have nonsynonymous mutations in the voltage-gated sodium channel (vgsc). We identified a leucine to phenylalanine mutation at position 1014 (L1014F) and a methionine to isoleucine mutation (M918I) of the A. glycines vgsc, both suspected of conferring knockdown resistance (kdr) to lambda-cyhalothrin. We developed molecular markers to identify these mutations in insecticide-resistant aphids. We determined that A. glycines which survived exposure to a diagnostic concentration of lambda-cyhalothrin and bifenthrin via glass-vial bioassays had these mutations, and showed significant changes in the resistance allele frequency between samples collected before and after field application of lambda-cyhalothrin. Thus, a strong association was revealed between aphids with L1014F and M918I vgsc mutations and survival following exposure to pyrethroids. Specifically, the highest survival was observed for aphids with the kdr (L1014F) and heterozygote super-kdr (L1014F + M918I) genotypes following laboratory bioassays and in-field application of lambda-cyhalothrin. These genetic markers could be used as a diagnostic tool for detecting insecticide-resistant A. glycines and monitoring the geographic distribution of pyrethroid resistance. We discuss how generating these types of data could improve our efforts to mitigate the effects of pyrethroid resistance on crop production.© 2022. The Author(s).
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\n Most studies of pesticide resistance have focused on the identification and functional analysis of resistance genes, but few studies have considered the signaling pathways involved in their regulation. In this work, we discovered that overexpression of a P450 that confers resistance to neonicotinoid insecticides in whitefly is\n trans\n -regulated by the transcription factor\n CREB\n. Further studies demonstrated that exposure to neonicotinoid insecticides activates a key pathway involved in the cellular response to extracellular signals, the MAPK signaling pathway, that activates\n CREB\n by phosphorylation.\n CREB\n then binds to a specific site on the promoter of\n CYP6CM1\n resulting in its increased expression. These findings reveal mechanisms underlying the regulation of P450-mediated pesticide resistance and also provide a potential target for pest control.\n
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