1. Academic Validation
  2. Dual interference with host neuropeptide signaling allows parasitoid wasp to hijack host sugar metabolism

Dual interference with host neuropeptide signaling allows parasitoid wasp to hijack host sugar metabolism

  • EMBO J. 2025 Nov 26. doi: 10.1038/s44318-025-00636-5.
Zhi-Zhi Wang # 1 2 3 4 Ruo-Fei Ma # 1 2 3 Li-Cheng Gu 1 2 3 Li-Zhi Wang 1 2 3 Ting Chen 1 2 3 Pei Yang 1 2 3 Jia-Ni Zou 1 2 3 Jiang-Yan Zhu 1 2 3 Zhi-Wei Wu 1 2 3 Yue-Nan Zhou 1 2 3 Min Shi 2 3 Xing-Xing Shen 1 2 3 Jian-Hua Huang 1 2 3 Xue-Xin Chen 5 6 7 8
Affiliations

Affiliations

  • 1 Institute of Insect Sciences, College of Agriculture and Biotechnology, Zhejiang University, Hangzhou, China.
  • 2 Ministry of Agriculture and Rural Affairs Key Lab of Molecular Biology of Crop Pathogens and Insect Pests, Zhejiang University, Hangzhou, China.
  • 3 Key Laboratory of Biology of Crop Pathogens and Insects of Zhejiang Province, Zhejiang University, Hangzhou, China.
  • 4 State Key Lab of Rice Biology and Breeding, Zhejiang University, Hangzhou, China.
  • 5 Institute of Insect Sciences, College of Agriculture and Biotechnology, Zhejiang University, Hangzhou, China. [email protected].
  • 6 Ministry of Agriculture and Rural Affairs Key Lab of Molecular Biology of Crop Pathogens and Insect Pests, Zhejiang University, Hangzhou, China. [email protected].
  • 7 Key Laboratory of Biology of Crop Pathogens and Insects of Zhejiang Province, Zhejiang University, Hangzhou, China. [email protected].
  • 8 State Key Lab of Rice Biology and Breeding, Zhejiang University, Hangzhou, China. [email protected].
  • # Contributed equally.
Abstract

Changes in host carbohydrate metabolism determine the outcome of host-parasite relationships, but the underlying mechanistic basis remains elusive. Here, we show that the parasitoid wasp Cotesia vestalis induces trehalose accumulation in its host, the moth Plutella xylostella, largely independently of Insulin/adipokinetic hormone signalling and food intake. Instead, parasitoids rewire host carbohydrate metabolism via two pathways activated by the evolutionarily conserved short neuropeptide F (sNPF), a functional analogue of mammalian neuropeptide Y. Parasitoid-derived teratocytes secrete sNPF that interacts with the sNPF receptor (sNPFR) on host cells, and contributes to host hypertrehalosemia by promoting glycogenolysis in the fat body. We further find that a parasitoid-symbiotic virus induces expression of host-encoded sNPF, which stimulates glycolysis in the host midgut. Furthermore, we show that the host sNPF-sNPFR complex stimulates Gq/CA2+ signalling, while the parasitoid sNPF, exhibiting higher receptor affinity, triggers Gi/cAMP signalling. Molecular docking analyses suggest that the observed distinct receptor activation properties may be attributed to structural variations in the sNPF-sNPFR binding pocket. Collectively, our findings uncover an unexpected role of peripheral sNPFs in the regulation of carbohydrate metabolism during host-parasite interactions.

Keywords

Host–parasite Interaction; Humoral Factor; Short Neuropeptide F; Sugar Metabolism.

Figures
Products