tca-miR-3835-5p-ACPR-ACC neuroendocrine axis controls locomotor behavior via lipid metabolism in Tribolium castaneum

Locomotor behavior is essential for insect survival, supporting activities such as foraging, mating, and predator avoidance. Neuropeptides are known to modulate movement, but the specific role of the adipokinetic hormone/corazonin-related peptide receptor (ACPR) in Tribolium castaneum remains unclear. Understanding how neuropeptide signaling integrates with energy metabolism to regulate locomotion may provide insights relevant to pest management.

RNAi-mediated knockdown of ACPR significantly impaired locomotor activity and depleted triacylglycerol (TAG) reserves, a primary energy source for sustained movement. ACPR silencing also reduced acetyl-CoA carboxylase (ACC) expression and malonyl-CoA levels, disrupting TAG biosynthesis. Additionally, tca-miR-3835-5p was identified as a post-transcriptional regulator of ACPR; injection of tca-miR-3835-5p mimics reproduced the effects of ACPR knockdown, including decreased ACC expression, malonyl-CoA deficiency and reduced locomotor performance. These results reveal a regulatory axis linking miRNA, neuropeptide signaling and lipid metabolism.

The tca-miR-3835-5p-ACPR-ACC pathway constitutes a novel molecular mechanism integrating neuroendocrine signaling with energy homeostasis to control locomotor behavior in T. castaneum. The present study not only advances understanding of the molecular and metabolic regulation of insect movement, but also identifies potential targets for sustainable pest management strategies aimed at disrupting energy-dependent behaviors. © 2026 Society of Chemical Industry.