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胰岛素/IGF 信号和 TORC1 通过诱导美洲大蠊的保幼激素生物合成来促进卵黄发生。

Insulin/IGF signaling and TORC1 promote vitellogenesis via inducing juvenile hormone biosynthesis in the American cockroach.

机构信息

Guangdong Provincial Key Laboratory of Insect Developmental Biology and Applied Technology, Institute of Insect Science and Technology and School of Life Sciences, South China Normal University, Guangzhou 510631, China.

Guangmeiyuan R&D Center, Guangdong Provincial Key Laboratory of Insect Developmental Biology and Applied Technology, South China Normal University, Meizhou 514779, China.

出版信息

Development. 2020 Oct 23;147(20):dev188805. doi: 10.1242/dev.188805.

DOI:10.1242/dev.188805
PMID:33097549
Abstract

Vitellogenesis, including vitellogenin (Vg) production in the fat body and Vg uptake by maturing oocytes, is of great importance for the successful reproduction of adult females. The endocrinal and nutritional regulation of vitellogenesis differs distinctly in insects. Here, the complex crosstalk between juvenile hormone (JH) and the two nutrient sensors insulin/IGF signaling (IIS) and target of rapamycin complex1 (TORC1), was investigated to elucidate the molecular mechanisms of vitellogenesis regulation in the American cockroach, Our data showed that a block of JH biosynthesis or JH action arrested vitellogenesis, in part by inhibiting the expression of (), a key transcription factor gene involved in the sex determination cascade. Depletion of IIS or TORC1 blocked both JH biosynthesis and vitellogenesis. Importantly, the JH analog methoprene, but not bovine insulin (to restore IIS) and amino acids (to restore TORC1 activity), restored vitellogenesis in the neck-ligated (IIS-, TORC1- and JH-deficient) and rapamycin-treated (TORC1- and JH-deficient) cockroaches. Combining classic physiology with modern molecular techniques, we have demonstrated that IIS and TORC1 promote vitellogenesis, mainly via inducing JH biosynthesis in the American cockroach.

摘要

卵黄发生包括脂肪体中卵黄蛋白原(Vg)的产生和成熟卵母细胞对 Vg 的摄取,对于成年雌性的成功繁殖至关重要。昆虫的卵黄发生在内分泌和营养调节方面有明显的不同。在这里,研究了保幼激素(JH)与两种营养传感器胰岛素/胰岛素样生长因子信号(IIS)和雷帕霉素复合物 1(TORC1)之间的复杂串扰,以阐明美洲大蠊卵黄发生调节的分子机制,我们的数据表明,JH 生物合成或 JH 作用的阻断部分通过抑制关键转录因子基因的表达而阻止卵黄发生,该基因参与性别决定级联反应。IIS 或 TORC1 的耗竭阻止了 JH 生物合成和卵黄发生。重要的是,JH 类似物保幼醚,而不是牛胰岛素(恢复 IIS)和氨基酸(恢复 TORC1 活性),可以恢复结扎颈(IIS-、TORC1-和 JH-缺乏)和雷帕霉素处理(TORC1-和 JH-缺乏)的美洲大蠊的卵黄发生。通过将经典生理学与现代分子技术相结合,我们证明 IIS 和 TORC1 促进卵黄发生,主要是通过在美洲大蠊中诱导 JH 生物合成。

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