The Tachinidae are natural enemies of many lepidopteran and coleopteran pests of crops, forests, and fruits. However, host-tachinid parasitoid interactions have been largely unexplored. In this study, we investigated the effects of tachinids on host biological traits, using Exorista japonica, a generalist parasitoid, and the silkworm Bombyx mori, its lepidopteran host, as models. We observed that E. japonica parasitoidism did not affect silkworm larval body weight gain and cocooning rate, whereas they caused shortened duration of molting from the final instar to the pupal stage, abnormal molting from larval to pupal stages, and a subsequent decrease in host emergence rate. Moreover, a decrease in juvenile hormone (JH) titer and an increase in 20-hydroxyecdysone (20E) titer in the hemolymph of parasitized silkworms occurred. The transcription of JH and 20E responsive genes was downregulated in mature parasitized hosts, but upregulated in parasitized prepupae while Fushi tarazu factor 1 (Ftz-f1), a nuclear receptor essential in larval ecdysis, showed dramatically reduced expression in parasitized hosts at both the mature and prepupal stages. Moreover, the transcriptional levels of BmFtz-f1 and its downstream target genes encoding cuticle proteins were downregulated in epidermis of parasitized hosts. Meanwhile, the content of trehalose was decreased in the hemolymph, while chitin content in the epidermis was increased in parasitized silkworm prepupae. These data reveal that the host may fine-tune JH and 20E synthesis to shorten developmental duration to combat established E. japonica infestation, while E. japonica silences BmFtz-f1 transcription to inhibit host pupation. This discovery highlights the novel target mechanism of tachinid parasitoids and provides new clues to host/tachinid parasitoid relationships.

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BACKGROUNDChlorantraniliprole (CAP) is widely used in agriculture and forestry to prevent and control pests. The effects of environmental CAP residue on non‐target insect metamorphosis have not been reported. Our research aimed to investigate the sublethal effect of CAP on larva–pupa transformation in silkworm, and explore the mechanism of sublethal CAP exposure‐mediated pupation metamorphosis defects.RESULTSublethal CAP exposure affected the growth and development of silkworm larvae and caused defects in pupation metamorphosis. After CAP exposure, formation the of prepupa procuticle, ecdysial membrane and new epidermis was inhibited. Also, the level of 20‐hydroxyecdysone (20E) and mRNA levels of the 20E signaling pathway‐related genes EcR, USP, E74, E75 and Ftz‐f1 were significantly reduced. Moreover, genes involved in chitin synthesis, such as ChsA, CDA1 and CDA2, were downregulated. Injection of 20E led to the upregulation of chitin synthesis‐related genes and increased formation of new epidermis in CAP‐treated silkworm. However, injection of 20E failed to prevent downregulation of Ftz‐f1 and the defects in pupation metamorphosis.CONCLUSIONOur results suggested that 20E is a target hormone of CAP exposure‐mediated epidermis formation phenotype. Ftz‐f1 was silenced by CAP and might be a direct target gene of sublethal CAP exposure. Our study provided new evidence of the effects of sublethal CAP exposure on insect development and metamorphosis. © 2020 Society of Chemical Industry

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