RNAi Suppression of Hormone Receptor HR3 Blocks Larval Molting and Metamorphosis in the Cigarette Beetle, <i>Lasioderma serricorne</i>

Abstract

Hormone receptor 3 (HR3), an early-late gene of the 20-hydroxyecdysone (20E) signaling pathway, plays a critical role in insect metamorphosis and development. In this study, we identified and characterized an HR3 gene (LsHR3) from the cigarette beetle, Lasioderma serricorne. The open reading frame of LsHR3 is 1581 bp encoding a 527 amino acid protein that contains a conserved DNA binding domain and a ligand binding domain. LsHR3 was mainly expressed in the fourth-instar larvae, prepupae, and pupae and showed high expression in the fat body. The expression of LsHR3 was induced by 20E, while it was significantly suppressed by silencing of six 20E synthesis and signaling pathway genes. RNA interference (RNAi)-aided knockdown of LsHR3 in the fourth-instar larvae disrupted the larval–pupal molting and caused 100% mortality. The 20E titer of LsHR3-depletion larvae was decreased, and expressions of five 20E synthesis genes were dramatically decreased. Silencing LsHR3 reduced chitin content and downregulated the expression of genes involved in chitin synthesis and degradation. Hematoxylin and eosin staining of abdominal cuticle showed that no apolysis occurred after silencing LsHR3. These results suggest that LsHR3-mediated 20E signaling is involved in the regulation of chitin metabolism during the molting process of L. serricorne, and targeting this gene by RNAi has potential in controlling this pest.

Keywords

• cigarette beetle
• hormone receptor
• molt
• 20-hydroxyecdysone
• chitin metabolism
• RNA interference