FTZ-F1 Homologue Silencing Reveals Endocrine and Xenobiotic-Response Vulnerabilities Associated with RNAi–Insect Growth Regulator Co-Treatment in Heortia vitessoides

Insect growth regulators disrupt endocrine signaling, but the molecular vulnerabilities underlying their effects remain incompletely understood. Here, two FTZ-F1 homologues in Heortia vitessoides were characterized and functionally analyzed. RNAi-mediated knockdown of either homologue impaired ecdysis, pupation, and adult emergence. HvFTZ-F1–1 knockdown was more strongly associated with reduced fat-body triglyceride content and lipid-metabolism-related transcription, whereas HvFTZ-F1–2 knockdown was more strongly associated with midgut epithelial disruption, reduced ELISA-derived 20E immunoreactive levels, and broader transcriptomic perturbation. Pyriproxyfen and tebufenozide induced opposite transcriptional responses of the two homologues. Chitosan-dsRNA cotreatment produced combination-dependent survival responses, with CS-dsF1+Teb and CS-dsF2+PPF showing reduced survival relative to the corresponding pesticide-control groups. These findings identify homologue-biased developmental vulnerabilities and support a laboratory framework for RNAi–insect growth regulator cotreatment in H. vitessoides.