RESUMEN
Environmental residues of pryriproxyfen, a juvenile hormone analogue (JHA) type pesticide, may have on unintended consequences on non-target insects. However, the mechanism of pyriproxyfen action and silk protein synthesis in silkworms has not been reported. In the present study, we treated the silkworms with trace pyriproxyfen (1 × 10-4 mg/L) and found that the silkworm larvae showed no obvious poisoning symptoms, while the development of silk glands and cocoon-forming function were both seriously damaged due to the accumulation of pyriproxyfen in posterior silk gland (PSG). The titer of the juvenile hormone (JH) was increased, whereas the content of 20-hydroxyecdysone (20E) was reduced in pyriproxyfen-exposed hemolymph. Met2 is a component of the JH receptor complex and JH can promote its phosphorylation. We found Met2 and SRC were up-regulated in the larval stage after pyriproxyfen exposure, the JH-Met2/SRC complex led to the up-regulation of downstream genes Kr-h1, and Dimm, and then specifically inhibited the transcription of Fib-H. Meanwhile, the transcription of ecdysone inducible transcription factor Br-C Z4 was also inhibited by pyriproxyfen and resulted in the defects of metamorphosis. In conclusion, the trace pyriproxyfen could affect the metamorphosis and silk protein synthesis through the Met2-mediated pathway. Our study provided new evidence that Met2 might be a potential target gene of JHA in Lepidoptera.