# Functional Characterization of Tachykinin in Regulating Feeding and Energy Metabolism in the Chinese Oak Silkworm, Antheraea pernyi

## TL;DR

This study shows that the tachykinin gene in the Chinese oak silkworm helps control feeding and energy storage, especially during hunger.

## Contribution

The study identifies and functionally characterizes the tachykinin gene in Antheraea pernyi for the first time.

## Key findings

- ApTK expression increases during starvation and decreases after refeeding, indicating a role in hunger signaling.
- Silencing ApTK leads to increased larval weight and higher energy storage levels.
- ApTK is mainly expressed in the brain and midgut and shares motifs with other insect tachykinins.

## Abstract

This study identified and characterized the tachykinin gene (ApTK) in the Chinese oak silkworm, Antheraea pernyi. ApTK encodes a peptide with four FX1GX2R motifs, where X1 and X2 represent variable amino acid residues, and is most highly expressed in the brain and midgut. Our results showed that ApTK expression increases during starvation and decreases after refeeding, indicating it responds to hunger. When ApTK was silenced using RNA interference, larvae gained more weight and had higher levels of triglyceride, glycogen, and trehalose. These findings demonstrate that ApTK acts to restrain feeding and limit energy storage, playing a key role in regulating energy balance in A. pernyi.

Tachykinins (TKs), a conserved family of neuropeptides, play critical roles in regulating multiple physiological processes such as feeding and energy metabolism in insects. This study identified the TK gene (ApTK) from the Chinese oak silkworm, Antheraea pernyi, an economically important insect species. Bioinformatic analysis showed that ApTK possesses four FX1GX2R motifs (X1 and X2 represent variable amino acid residues), comprising FMGVR, FYGVR, FIGVR, and FFGMR, in the C-terminus and shares a close phylogenetic relationship with TKs from Bombyx mori and Manduca sexta. Tissue-specific expression profiling demonstrated that ApTK was mainly expressed in the brain and midgut. Starvation–refeeding experiments showed that the expression of ApTK was significantly upregulated during food deprivation and returned to baseline after refeeding, evincing its involvement in hunger signaling. RNA interference (RNAi)-mediated knockdown of ApTK led to a significant increase in larval body weight and increased levels of triglyceride, glycogen, and trehalose, indicating enhanced energy storage. Collectively, these results demonstrate that ApTK acts as a key regulator in restraining feeding and modulating energy homeostasis in A. pernyi. Our findings provide insights into the neuroendocrine mechanisms underlying feeding behavior and energy metabolism in A. pernyi.