A pesticide hijacks a neurohormonal circuit to block ovulation in insects

Authors

Xing, J.-Y., Su, S., Lin, P.-X., Guo, Y., Wu, D.-R., Li, R.-A., Nassel, D. R., Bass, C., Gao, C.-F., Wu, S.-F.

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.

Preprint server: bioRxiv
The authors list and abstract were imported from bioRxiv on 07 Jul 2026.

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