The Ecdysone and Notch Pathways Synergistically Regulate Cut at the Dorsal-Ventral Boundary in Drosophila Wing Discs.
The Ecdysone and Notch Pathways Synergistically Regulate Cut at the Dorsal-Ventral Boundary in Drosophila Wing Discs.
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DOI：
10.1016/j.jgg.2016.03.002
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发表时间：
2016-04-20
期刊：
影响因子：
--
通讯作者：
Deng WM
中科院分区：
文献类型：
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作者：
Jia D;Bryant J;Jevitt A;Calvin G;Deng WM
后生动物的发育需要协调信号通路来调节基因表达模式。在果蝇中，翅膀想象盘为研究信号通路如何相互作用以调节模式形成提供了一个很好的模型。翅盘背/腹侧（DV）边界的确定取决于Notch通路，该通路沿DV边界被激活并诱导同源盒转录因子Cut的表达。在这里，我们发现锌指转录因子Broad （Br）也参与调节DV边界区Cut的表达。然而，Br的表达不受翼盘Notch信号的调控，相反，ecdysone信号是诱导Br上调Cut的上游信号。此外，我们发现ecdysone- br级联上调cut- lacz的表达，这是一个包含2.7 kb切割增强子区域的报告子，这意味着ecdysone信号传导与Notch类似，在转录水平上调节切割。总的来说，我们的研究结果表明Notch和ecdysone信号通路协同调节Cut表达，以促进翼盘中DV边界的形成。此外，我们发现br在DV边界附近促进Notch配体Delta抑制异常的高Notch活性，这表明两种途径之间存在进一步的相互作用，导致翼盘DV图案。
Metazoan development requires coordination of signaling pathways to regulate patterns of gene expression. In Drosophila, the wing imaginal disc provides an excellent model for the study of how signaling pathways interact to regulate pattern formation. The determination of the dorsal/ventral (DV) boundary of the wing disc depends on the Notch pathway, which is activated along the DV boundary and induces the expression of the homeobox transcription factor, Cut. Here, we show that Broad (Br), a zinc-finger transcription factor, is also involved in regulating Cut expression in the DV boundary region. However, Br expression is not regulated by Notch signaling in wing discs, rather, ecdysone signaling is the upstream signal that induces Br for Cut upregulation. Also, we find that the ecdysone-Br cascade upregulates cut-lacZ expression, a reporter containing a 2.7 kb cut enhancer region, implying that ecdysone signaling, similar to Notch, regulates cut at the transcriptional level. Collectively, our findings reveal that the Notch and ecdysone signaling pathways synergistically regulate Cut expression for proper DV boundary formation in the wing disc. Additionally, we show br promotes Delta, a Notch ligand, near the DV boundary to suppress aberrant high Notch activity, indicating further interaction between the two pathways for DV patterning of the wing disc.