A pesticide hijacks a neurohormonal circuit to block ovulation in insects

Abstract

The global decline of insect populations threatens ecosystem stability, yet the hidden physiological impacts of sublethal pesticide exposure remain largely uncharted. Here we show that emamectin benzoate (EB), a widely used insecticide, suppresses female fertility not by disrupting egg development, but by specifically blocking ovulation. Through a systematic genetic screen in Drosophila, we identify the glutamate-gated chloride channel GluCl in a discrete set of octopaminergic neurons as the primary neural target. EB subverts the activity of this circuit, thereby impairing octopamine-dependent follicle rupture, suppressing ovarian ecdysteroid signaling, and altering oviduct muscle dynamics--three coordinated processes essential for egg release. Strikingly, this ovulatory blockade is recapitulated in diverse dipteran pests and disease-vector mosquitoes, revealing a conserved vulnerability. Our findings establish a neurohormonal mechanism by which a common agrochemical hijacks reproductive control, and they expose ovulation as a critical, hitherto unrecognized nexus between environmental chemicals and insect population dynamics. SignificanceSublethal pesticide exposure can profoundly alter insect physiology beyond acute toxicity, yet the underlying mechanisms remain unclear. Here, we show that emamectin benzoate (EB), a widely used avermectin insecticide, suppresses ovulation and female fecundity in Drosophila by disrupting octopaminergic signaling, follicle rupture, and oviduct muscle contraction. Mechanistically, EB acts through GluCl-dependent neural pathways to impair ovulation-related processes and reproductive muscle dynamics. Notably, these inhibitory effects are conserved across multiple dipteran species, suggesting that reproductive suppression represents a broader physiological consequence of EB exposure. Our findings reveal a previously unrecognized neuro-reproductive mechanism of pesticide action and provide new insight into how sublethal insecticide exposure may influence insect population dynamics.