Buprofezin affects the molting process by regulating nuclear receptors SfHR3 and SfHR4 in Sogatella furcifera.

Nuclear receptors play a crucial role in various signaling and metabolic pathways, such as insect molting and development. Buprofezin (2-tert-butylimino-3-isopropyl-5-phenyl-perhydro-1, 3, 5-thiadiazin-4-one), a chitin synthesis inhibitor, causes molting deformities and slow death in insects by inhibiting chitin synthesis and interfering with their metabolism. This study investigated whether buprofezin affects insect ecdysteroid signaling pathway. The treatment of buprofezin significantly suppressed the transcription levels of SfHR3 and SfHR4, two nuclear receptor genes, in third-instar nymphs of Sogatella furcifera. Meanwhile, the transcription levels of SfHR3 and SfHR4 in first-day fifth-instar nymphs were induced at 12 h after 20E treatment. In addition, the silencing of SfHR3 and SfHR4 genes in first-day fifth-instar nymphs caused severe developmental delay and molting failure, resulting in a significant reduction of survival rates at 7.36% and 2.99% on the eighth day, respectively. Further analysis showed that the silencing SfHR3 and SfHR4 significantly inhibited the transcription levels of chitin synthesis and degradation-related genes. These results indicate that buprofezin can inhibits chitin synthesis and degradation by suppressing the signal transduction of 20E through SfHR3 and SfHR4, leading to molting failure and death. This study not only expands our understanding of the molecular mechanism of buprofezin in pest control but also lays a foundation for developing new control strategies of RNAi by targeting SfHR3 and SfHR4.
Competing Interests: Declaration of Competing Interest The authors declare that they have no conflicts of interest in regard to the contents of this article.
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