The neonicotinoid imidacloprid impairs the predatory performance and functional response of the jumping spider Helpis minitabunda (Araneae, Salticidae)

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  The neonicotinoid imidacloprid impairs the predatory performance and functional response of the jumping spider Helpis minitabunda (Araneae, Salticidae) Abstract The neonicotinoid imidacloprid can cause lethal and sublethal effects in non-target organisms, including impaired behavior, reduced fertility, disrupted locomotion, and reduced predatory performance in arthropods. Spiders are among the most abundant arthropod predators in terrestrial ecosystems, including agricultural ecosystems, yet the effects of neonicotinoids on the predatory function of jumping spiders remain poorly understood. The functional response of a predator describes how predation rates change with prey density and is key to understanding predator–prey dynamics. We tested whether acute exposure to a commercial formulation of imidacloprid at field-recommended concentrations alters the functional response of the Aussie bronze jumping spider, Helpis minitabunda (L. Koch, 1880). We compared the predation of treat...

Characterization of the mechanism of action of a re-engineered spider toxin acting on insect voltage-gated sodium channels

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Characterization of the mechanism of action of a re-engineered spider toxin acting on insect voltage-gated sodium channels

Abstract

Insect resistance to conventional chemical insecticides, such as knockdown resistance (kdr) to pyrethroids, poses a growing challenge to effective pest control globally. Spider venoms are an exceptionally rich source of insecticidal peptide toxins with significant potential for development into bioinsecticides for agricultural applications and human disease vector control. The spider Pireneitega luctuosa produces four insecticidal δ-Amaurobitoxin-Pl1 toxins, Pl1a-d. Pl1a and Pl1b were reported to act on voltage-gated sodium channels from several studies; however, the mechanism of action remains controversial. Furthermore, the action of Pl1c and Pl1d has not been examined. In this study, the effects of Pl1c and its re-engineered derived peptide with improved production yield, VSE-8419, on the cockroach sodium channel BgNav1–1a were compared in Xenopus oocytes using two-electrode voltage clamp. While improved production yield of VSE-8419 costed potency, both VSE-8419 and Pl1c still drastically shifted the voltage dependence of activation in the hyperpolarizing direction (∼-30 mV shift), promoting sodium channel activation, a typical action of site 4 neurotoxins. Strikingly, VSE-8419 and Pl1c are more potent gating modifiers of sodium channels in the inactivated state (EC50: VSE-8419 = 651.80 nM; Pl1c = 186.69 nM) than in the resting or open states. Furthermore, VSE-8419 is active against pyrethroid-resistant sodium channels carrying kdr mutations that reside within or outside of the two predicted pyrethroid receptor sites. Our findings elucidate the mechanism of action of Pl1c and VSE-8419, on insect sodium channels and highlight their potential as alternative agents to manage pests and human disease vectors, including pyrethroid-resistant pest/vector populations.
Andreazza, F., Valbon, W., Tourtois, J., Flohrschutz, C., Bell, L., Schneider, K., Bao, L., & Dong, K. (2026). Characterization of the mechanism of action of a re-engineered spider toxin acting on insect voltage-gated sodium channels. Pesticide Biochemistry and Physiology, 216, 106748. https://doi.org/10.1016/j.pestbp.2025.106748