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首页> 美国卫生研究院文献>The Journal of Biological Chemistry >20-Hydroxyecdysone (20E) Primary Response Gene E93 Modulates 20E Signaling to Promote Bombyx Larval-Pupal Metamorphosis
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20-Hydroxyecdysone (20E) Primary Response Gene E93 Modulates 20E Signaling to Promote Bombyx Larval-Pupal Metamorphosis

机译：20羟蜕皮激素（20E）初级反应基因E93调节20E信号传导促进家蚕幼虫-的变态

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As revealed in a previous microarray study to identify genes regulated by 20-hydroxyecdysone (20E) and juvenile hormone (JH) in the silkworm, Bombyx mori, E93 expression in the fat body was markedly low prior to the wandering stage but abundant during larval-pupal metamorphosis. Induced by 20E and suppressed by JH, E93 expression follows this developmental profile in multiple silkworm alleles. The reduction of E93 expression by RNAi disrupted 20E signaling and the 20E-induced autophagy, caspase activity, and cell dissociation in the fat body. Reducing E93 expression also decreased the expression of the 20E-induced pupal-specific cuticle protein genes and prevented growth and differentiation of the wing discs. Importantly, the two HTH domains in E93 are critical for inducing the expression of a subset of 20E response genes, including EcR, USP, E74, Br-C, and Atg1. By contrast, the LLQHLL and PLDLSAK motifs in E93 inhibit its transcriptional activity. E93 binds to the EcR-USP complex via a physical association with USP through its LLQHLL motif; and this association is enhanced by 20E-induced EcR-USP interaction, which attenuates the transcriptional activity of E93. E93 acts through the two HTH domains to bind to GAGA-containing motifs present in the Atg1 promoter region for inducing gene expression. In conclusion, E93 transcriptionally modulates 20E signaling to promote Bombyx larval-pupal metamorphosis.
机译：正如先前的一项微阵列研究所揭示的那样，该研究旨在鉴定家蚕Bombyx mori中受20-羟基蜕皮激素（20E）和少年激素（JH）调控的基因，在E游阶段之前，脂肪体内的E93表达明显较低，而在幼虫期则较高。 meta变态。受20E诱导并受JH抑制，E93表达在多个家蚕等位基因中遵循此发育模式。 RNAi引起E93表达的降低破坏了20E信号传导以及20E诱导的自噬，胱天蛋白酶活性和脂肪体内的细胞解离。减少E93表达还降低了20E诱导的p特异性角质层蛋白基因的表达，并阻止了翼盘的生长和分化。重要的是，E93中的两个HTH结构域对于诱导20E反应基因子集的表达至关重要，包括EcR，USP，E74，Br-C和Atg1。相比之下，E93中的LLQHLL和PLDLSAK基序抑制了其转录活性。 E93通过其LLQHLL基序与USP物理结合，从而与EcR-USP复合物结合； 20E诱导的EcR-USP相互作用增强了这种联系，从而减弱了E93的转录活性。 E93通过两个HTH结构域与Atg1启动子区域中存在的含GAGA的基序结合，以诱导基因表达。总之，E93转录​​调节20E信号传导，以促进Bombyx幼虫-pu变态。

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