Molecular mechanisms of phosphocholine cytidylyltransferase and phosphoethanolamine cytidylyltransferase in regulating survival and lipid homeostasis in Nilaparvata lugens.

Abstract

Phosphocholine cytidylyltransferase (CCT) and phosphoethanolamine cytidylyltransferase (ECT) are key enzymes in glycerophospholipid metabolism. They not only participate in the Kennedy pathway for phosphatidylcholine (PC) and phosphatidylethanolamine (PE) synthesis but also indirectly regulate triglyceride (TG) and cholesterol metabolism, contributing to lipid homeostasis. In this study, we revealed the roles of NlCCT and NlECT in the growth and lipid metabolism of Nilaparvata lugens. Despite conserved domains, RNAi knockdown of NlCCT or NlECT caused distinct phenotypes: both reduced survival, while dsNlECT also led to molting failure, increased body weight, and elevated TG levels. Lipidomics of dsNlECT-treated insects identified 86 significantly altered metabolites across nine lipid classes, mainly enriched in glycerophospholipid metabolism and TG biosynthesis pathways. RT-qPCR further validated 15 key metabolic enzyme genes correlated with these lipid changes. Notably, NlCCT expression was suppressed after NlECT knockdown, indicating close functional crosstalk. These results suggest that CCT and ECT coordinately regulate lipid homeostasis via a complex metabolic network in N. lugens. These findings highlight the critical roles of NlCCT and NlECT in regulating lipid metabolism in N. lugens, providing novel insights into the lipid metabolic network in insects and offering a theoretical foundation for the development of environmentally friendly pest control strategies targeting lipid metabolic pathways.