Silencing uridine diphosphate N‐acetylglucosamine pyrophosphorylase gene impairs larval development in Henosepilachna vigintioctopunctata

BACKGROUND Uridine diphosphate‐N‐acetylglucosamine (UDP‐GlcNAc) diphosphorylase (UAP) catalyzes the formation of UDP‐GlcNAc, the precursor for the production of chitin in ectodermally derived epidermal cells and midgut, for GlcNAcylation of proteins and for generation of glycosyl‐phosphatidyl‐inositol anchors in all tissues in Drosophila melanogaster. RESULTS Here, we identified a putative HvUAP gene in Henosepilachna vigintioctopunctata. Knockdown of HvUAP at the second‐, third‐ and fourth‐instar stages impaired larval development. Most resultant HvUAP hypomorphs showed arrested development at the third‐, fourth‐instar larval or prepupal stages, and became paralyzed, depending on the age when treated. Some HvUAP‐silenced larvae had weak and soft scoli. A portion of HvUAP‐depleted beetles formed misshapen pupae. No HvUAP RNA interference pupae successfully emerged as adults. Dissection and microscopic observation revealed that knockdown of HvUAP affected gut growth and food ingestion, reduced cuticle thickness, and negatively affected the formation of newly generated cuticle layers during ecdysis. Furthermore, HvUAP deficiency inhibited development of the tracheal respiratory system and thinned tracheal taenidia. CONCLUSION The phenotypical defects in HvUAP hypomorphs suggest that HvUAP is involved in the production of chitin. Moreover, our findings will enable the development of a double‐stranded RNA‐based pesticide to control H. vigintioctopunctata. © 2021 Society of Chemical Industry. Knockdown of HvUAP impairs larval development in Henosepilachna vigintioctopunctata. HvUAP hypomorphs become paralyzed. HvUAP‐depleted larvae have weak and soft scoli. Silencing HvChSA influences gut structure and cuticle formation. Depletion of HvChSA inhibits trachea generation and thins tracheal taenidia.