CarE1 and GST1 Are Involved in Beta-Cypermethrin Resistance in Field Populations of the Mirid Bug, Apolygus lucorum

TL;DR

The mirid bug Apolygus lucorum has developed resistance to the insecticide beta-cypermethrin, primarily through increased activity of detoxification genes CarE1 and GST1.

Contribution

This study identifies CarE1 and GST1 as key genes contributing to beta-cypermethrin resistance in A. lucorum, offering new insights for pest control strategies.

Findings

Field populations of A. lucorum showed significantly higher survival rates after insecticide exposure compared to laboratory strains.

RNAi silencing of CarE1 and GST1 increased susceptibility to beta-cypermethrin in field populations.

CarE1 and GST1 are overexpressed in field populations, correlating with increased resistance.

Abstract

The mirid bug Apolygus lucorum has become an important pest in cotton cultivation, especially due to the widespread cultivation of Bt cotton. This species of insect bug has developed increasing resistant to insecticides, posing a growing threat to agriculture. In the present study, we investigated the mechanism underlying its resistance to beta-cypermethrin. We discovered that a field-collected population of A. lucorum survived insecticide exposure at significantly higher rates than the laboratory sensitive strain. The resistance is associated with increased expression levels of two detoxification genes, CarE1 and GST1. Silencing these genes increased the susceptibility of pests to insecticides. Our results demonstrate that CarE1 and GST1 are key contributors to beta-cypermethrin resistance in A. lucorum, providing new insights for developing safer and effective pest control strategies.

The widespread cultivation of transgenic Bt cotton has elevated Apolygus lucorum (Meyer-Dür) to a major pest in cotton agroecosystems. Its rapidly developing resistance to insecticides poses a serious challenge to sustainable agriculture. In this study, we assessed the susceptibility of a field-collected population from Anyang, Henan Province, in relation to a laboratory-susceptible strain, to elucidate the present status and molecular basis of resistance to beta-cypermethrin. First, the toxicity of beta-cypermethrin to A. lucorum was assessed through a diet-incorporation method. Subsequently, the enzymatic activities of carboxylesterase (CarE) and glutathione S-transferase (GST) were measured, and the expression levels of CarE1 and GST1 were quantified by quantitative real-time PCR (qRT-PCR). Finally, the function of candidate genes was confirmed using RNA interference (RNAi) technology. The bioassays results indicated that the median lethal concentration (LC50) for the laboratory and Anyang field strain were 343.34 mg/L and 700.45 mg/L, respectively. Following 48 h of exposure to the LC30 of the susceptible strain, the mortality rate of the field population (20.00%) was significantly lower than that of the laboratory population (33.33%), suggesting an increase in resistance. The field population of A. lucorum exhibited significantly higher activities of CarE (1.61-fold) and GST (1.71-fold) compared to the laboratory strain, accompanied by 3.63- and 4.23-fold overexpression of the corresponding genes CarE1 and GST1. Spatiotemporal expression profiling revealed that CarE1 expression was highest in 4th–5th instar nymphs and adults, with predominant localization in the midgut, while GST1 expression peaked in 4th–5th instar nymphs and was abundant in the midgut and fat body. RNAi-mediated knockdown of CarE1 and GST1 significantly enhanced susceptibility to beta-cypermethrin in field populations, resulting in elevated mortality 48 h post-treatment compared to controls. In conclusion, the field population of A. lucorum has developed considerable resistance to beta-cypermethrin, strongly correlated with overexpression of CarE1 and GST1. These results deepen our understanding of metabolic resistance mechanisms and offer valuable insights for developing targeted pest control strategies.

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