College of Agriculture, Guangxi University, Nanning, Guangxi 530004, PR China.
College of Agriculture, Guangxi University, Nanning, Guangxi 530004, PR China; Guangxi Key Laboratory of Agro-Environment and Agric-Products Safety, National Demonstration Center for Experimental Plant Science Education, College of Agriculture, Guangxi University, Nanning, Guangxi 530004, PR China.
Pestic Biochem Physiol. 2024 Nov;205:106139. doi: 10.1016/j.pestbp.2024.106139. Epub 2024 Sep 18.
The neuropeptide prothoracicotropic hormone (PTTH) plays a key role in regulating ecdysone synthesis and promoting insect metamorphosis. Pyriproxyfen is a juvenile hormone analogue. We previously reported that pyriproxyfen disrupts ecdysone secretion and inhibits larval-pupal metamorphosis in silkworms. However, the specific molecular mechanisms by which pyriproxyfen interferes with ecdysone signaling remain to be elucidated. Herein, the RNA-seq analysis on the ecdysone-secretion organ prothoracic gland (PG) was conducted following pyriproxyfen exposure. A total of 3774 differentially expressed genes (DEGs) were identified, with 1667 up-regulated and 2107 down-regulated. KEGG analysis showed that DEGs were enriched in the MAPK signaling pathway, a conserved pathway activated by PTTH binding to Torso, which regulates the ecdysone synthesis. qRT-PCR results indicated a significant up-regulation in PTTH transcription level, while the transcription levels of torso and downstream MAPK pathway genes, Ras2, Raf and ERK, were down-regulated 24 h post-pyriproxyfen treatment. Consistent with these transcriptional changes, PTTH titers in the brain also increased following pyriproxyfen treatment. These results suggest that pyriproxyfen induces abnormal metamorphosis in silkworms by impairing PTTH-Torso signaling. This study enhances our understanding of the molecular mechanisms of pyriproxyfen-induced larval-pupal abnormal metamorphosis in silkworms, and also provides insights for developing detoxification strategies for juvenile hormone analog pesticides to non-target organisms.
神经肽促前胸腺激素 (PTTH) 在调节蜕皮激素合成和促进昆虫变态中起着关键作用。吡丙醚是一种保幼激素类似物。我们之前报道过，吡丙醚会破坏蜕皮激素的分泌并抑制家蚕幼虫化蛹变态。然而，吡丙醚干扰蜕皮激素信号的具体分子机制仍有待阐明。在此，我们对蜕皮激素分泌器官前胸腺（PG）进行了吡丙醚暴露后的 RNA-seq 分析。共鉴定出 3774 个差异表达基因（DEGs），其中 1667 个上调，2107 个下调。KEGG 分析表明，DEGs 富集在 MAPK 信号通路中，该通路是由 PTTH 与 Torso 结合激活的保守通路，调节蜕皮激素的合成。qRT-PCR 结果表明 PTTH 转录水平显著上调，而 torso 和下游 MAPK 通路基因 Ras2、Raf 和 ERK 的转录水平在吡丙醚处理 24 小时后下调。与这些转录变化一致，吡丙醚处理后脑中的 PTTH 滴度也增加。这些结果表明，吡丙醚通过破坏 PTTH-Torso 信号诱导家蚕异常变态。本研究加深了我们对吡丙醚诱导家蚕幼虫化蛹异常变态的分子机制的理解，也为开发针对非靶标生物的保幼激素类似农药解毒策略提供了思路。
