A CREB-binding site as a target for decapentaplegic signalling during Drosophila endoderm induction
A CREB-binding site as a target for decapentaplegic signalling during Drosophila endoderm induction
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DOI：
10.1093/emboj/16.8.2014
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发表时间：
1997-04-15
期刊：
影响因子：
11.4
通讯作者：
Bienz, M
中科院分区：
文献类型：
--
作者：
Eresh, S;Riese, J;Bienz, M
Decapentaplegic（Dpp）是转化生长因子β家族的一种细胞外信号，在果蝇发育过程中具有多种功能。例如，它在内胚层诱导过程中在胚胎中起关键作用。在此过程中，Dpp刺激内脏中胚层中的同源异型基因Ultrabithorax和下下内胚层中的唇基因的转录。在这里，我们表明，cAMP反应元件（CRE）从Ultrabithorax增强子介导的Dpp响应转录在胚胎中肠，和内胚层表达从唇增强子依赖于多个克雷斯。此外，果蝇的CRE结合蛋白dCREB-B结合的Ultrabithorax的CRE，和无处不在的显性负性形式的dCREB-B的表达抑制CRE介导的报告基因的表达，并减少唇内胚层的表达。因此，CREB蛋白可以作为一个核目标，或作为一个合作伙伴的核目标，Dpp信号在胚胎中肠。
Decapentaplegic (Dpp) is an extracellular signal of the transforming growth factor-beta family with multiple functions during Drosophila development. For example, it plays a key role in the embryo during endoderm induction. During this process, Dpp stimulates transcription of the homeotic genes Ultrabithorax in the visceral mesoderm and labial in the subjacent endoderm. Here, we show that a cAMP response element (CRE) from an Ultrabithorax enhancer mediates Dpp-responsive transcription in the embryonic midgut, and that endoderm expression from a labial enhancer depends on multiple CREs. Furthermore, the Drosophila CRE-binding protein dCREB-B binds to the Ultrabithorax CRE, and ubiquitous expression of a dominant-negative form of dCREB-B suppresses CRE-mediated reporter gene expression and reduces labial expression in the endoderm. Therefore, a CREB protein may act as a nuclear target, or as a partner of a nuclear target, for Dpp signalling in the embryonic midgut.