Cyclic adenosine monophosphate (cAMP) response element binding protein (CREB)‐binding protein (CBP or CREBBP) plays important roles in regulating gene transcription and animal development. However, the process by which CBP is up‐regulated to impact insect development is unknown. In this study, the regulatory mechanism of Bombyx mori CBP (BmCBP) expression induced by 20‐hydroxyecdysone (20E) was investigated. In the Bo. mori cell line, DZNU‐Bm‐12, 20E enhanced BmCBP transcription and histone H3K27 acetylation. BmCBP RNA interference (RNAi) resulted in decreased histone H3K27 acetylation. Additionally, the luciferase activity analysis revealed that the transcription factor, Bo. mori CCAAT/enhancer‐binding protein gamma (BmC/EBPg), activated BmCBP transcription, which was suppressed by BmC/EBPg RNAi and promoted by BmC/EBPg overexpression. Electrophoretic mobility shift assay and chromatin immunoprecipitation results demonstrated that BmC/EBPg could bind to the C/EBP cis‐regulatory elements in two positions of the BmCBP promoter. Moreover, BmC/EBPg transcription was enhanced by the 20E receptor (BmEcR), which bound to the BmC/EBPg promoter. BmEcR RNAi significantly inhibited the transcriptional levels of BmC/EBPg and BmCBP in the presence of 20E. Furthermore, the BmEcR‐BmC/EBPg pathway regulated the acetylation levels of histone H3K27. Altogether, these results indicate that BmEcR enhances the expression of BmC/EBPg, which binds to the BmCBP promoter, activates BmCBP expression and leads to histone H3K27 acetylation.

中文翻译：

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20-羟基蜕皮激素受体激活的家蚕CCAAT /增强子结合蛋白γ调节Bo中BmCBP的表达和随后的组蛋白H3赖氨酸27乙酰化。森

环状单磷酸腺苷（cAMP）反应元件结合蛋白（CREB）结合蛋白（CBP或CREBBP）在调节基因转录和动物发育中起重要作用。但是，尚不清楚CBP上调影响昆虫发育的过程。本研究探讨了20-羟基蜕皮激素（20E）诱导家蚕 CBP（BmCBP）表达的调控机制。在博。mori细胞系DZNU‐Bm‐ 12、20E增强了BmCBP转录和组蛋白H3K27乙酰化作用。BmCBP RNA干扰（RNAi）导致组蛋白H3K27乙酰化降低。此外，萤光素酶活性分析显示转录因子Bo。森CCAAT /增强子结合蛋白γ（BmC / EBPg）激活了BmCBP转录，该转录受BmC / EBPg RNAi抑制并由BmC / EBPg过表达促进。电泳迁移率变动分析和染色质免疫沉淀结果表明，BmC / EBPg可以在BmCBP启动子的两个位置与C / EBP顺式调控元件结合。此外，BmC / EBPg转录被20E受体（BmEcR）增强，该受体与BmC / EBPg启动子结合。BmEcR RNAi显着抑制BmC / EBPg和BmCBP的转录水平在20E的情况下。此外，BmEcR-BmC / EBPg途径调节组蛋白H3K27的乙酰化水平。总而言之，这些结果表明BmEcR增强了与BmCBP启动子结合的BmC / EBPg的表达，激活了BmCBP的表达并导致了组蛋白H3K27的乙酰化。