Abstract

Simple SummaryThe dipteran parasitoid Tachinidae are important biocontrol agents and some of them are pests in sericulture. We previously have demonstrated that tachinid parasitoid Exorista japonica parasitism causes pupation defects in Bombyx mori. However, the underlying mechanism is not fully understood. In this study, we performed transcriptome analysis of the fat body of B. mori parasitized by E. japonica. We found that the host basal metabolism was inhibited whereas the immune response was activated. These results indicate that the tachinid parasitoid perturbs the basal metabolism and activates the energetically costly immunity of the host, leading to the development arrest of the host. This study provides insights into how tachinid parasitoids modify host basal metabolism and immune response for the benefit of developing parasitoid larvae.The dipteran tachinid parasitoids are important biocontrol agents, and they must survive the harsh environment and rely on the resources of the host insect to complete their larval stage. We have previously demonstrated that the parasitism by the tachinid parasitoid Exorista japonica, a pest of the silkworm, causes pupation defects in Bombyx mori. However, the underlying mechanism is not fully understood. Here, we performed transcriptome analysis of the fat body of B. mori parasitized by E. japonica. We identified 1361 differentially expressed genes, with 394 genes up-regulated and 967 genes down-regulated. The up-regulated genes were mainly associated with immune response, endocrine system and signal transduction, whereas the genes related to basal metabolism, including energy metabolism, transport and catabolism, lipid metabolism, amino acid metabolism and carbohydrate metabolism were down-regulated, indicating that the host appeared to be in poor nutritional status but active in immune response. Moreover, by time-course gene expression analysis we found that genes related to amino acid synthesis, protein degradation and lipid metabolism in B. mori at later parasitization stages were inhibited. Antimicrobial peptides including Cecropin A, Gloverin and Moricin, and an immulectin, CTL11, were induced. These results indicate that the tachinid parasitoid perturbs the basal metabolism and induces the energetically costly immunity of the host, and thus leading to incomplete larval–pupal ecdysis of the host. This study provided insights into how tachinid parasitoids modify host basal metabolism and immune response for the benefit of developing parasitoid larvae.

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