Characterization and functional analysis of chitinase family genes involved in nymph-adult transition ofSogatella furcifera

Chitinase degrades chitin in the old epidermis or peritrophic matrix of insects, which ensures normal development and metamorphosis. In our previous work, we comprehensively studied the function ofSfCht7inSogatella furcifera. However, the number and function of chitinase genes inS.furciferaremain unknown. Here, we identified 12 full-length chitinase transcripts fromS.furcifera, which included nine chitinase (Cht), two imaginal disc growth factor (IDGF), and one endo-beta-N-acetylglucosaminidase (ENGase) genes. Expression analysis results revealed that the expression levels of eight genes (SfCht3,SfCht5,SfCht6-1,SfCht6-2,SfCht7,SfCht8,SfCht10, andSfIDGF2) with similar transcript levels peaked prior to molting of each nymph and were highly expressed in the integument. Based on RNA interference (RNAi), description of the functions of each chitinase gene indicated that the silencing ofSfCht5,SfCht10, andSfIDGF2led to molting defects and lethality. RNAi inhibited the expressions ofSfCht5,SfCht7,SfCht10, andSfIDGF2, which led to downregulated expressions of chitin synthase 1 (SfCHS1,SfCHS1a, andSfCHS1b) and four chitin deacetylase genes (SfCDA1,SfCDA2,SfCDA3, andSfCDA4), and caused a change in the expression level of two trehalase genes (TRE1andTRE2). Furthermore, silencing ofSfCht7induced a significant decrease in the expression levels of three wing development-related genes (SfWG,SfDpp, andSfHh). In conclusion,SfCht5,SfCht7,SfCht10, andSfIDGF2play vital roles in nymph-adult transition and are involved in the regulation of chitin metabolism, andSfCht7is also involved in wing development; therefore, these genes are potential targets for control ofS.furcifera.

Automated summary

Twelve full-length chitinase transcripts were identified from S. furcifera, with eight genes showing peak expression levels before each nymph molting, primarily highly expressed in the integument, while silencing of SfCht5, SfCht10, and SfIDGF2 genes resulted in molting defects and lethality.