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首页> 外文期刊>Molecular and Cellular Biology >Nuclear Factor 1 and T-Cell Factor/LEF Recognition Elements Regulate Pitx2 Transcription in Pituitary Development
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Nuclear Factor 1 and T-Cell Factor/LEF Recognition Elements Regulate Pitx2 Transcription in Pituitary Development

机译：核因子1和T细胞因子/ LEF识别元件调节垂体发育中的Pitx2转录。

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Pitx2, a paired-related homeobox gene that is mutated in Rieger syndrome I, is the earliest known marker of oral ectoderm. Pitx2 was previously shown to be required for tooth, palate, and pituitary development in mice; however, the mechanisms regulating Pitx2 transcription in the oral ectoderm are poorly understood. Here we used an in vivo transgenic approach to investigate the mechanisms regulating Pitx2 transcription. We identified a 7-kb fragment that directs LacZ expression in oral ectoderm and in many of its derivatives. Deletion analysis of transgenic embryos reduced this fragment to a 520-bp region that directed LacZ activity to Rathke's pouch. A comparison of the mouse and human sequences revealed a conserved nuclear factor 1 (NF-1) recognition element near a consensus T-cell factor (TCF)/LEF binding site. The mutation of either site individually abolished LacZ activity in transgenic embryos, identifying Pitx2 as a direct target of Wnt signaling in pituitary development. These findings uncover a requirement for NF-1 and TCF factors in Pitx2 transcriptional regulation in the pituitary and provide insight into the mechanisms controlling region-specific transcription in the oral ectoderm and its derivatives.
机译： Pitx2 是成对的同源盒基因，在里格综合征I中发生了突变，是已知的最早的口腔外胚层标记。先前显示， Pitx2 是小鼠牙齿，上颚和垂体发育所必需的。然而，对口腔外胚层中 Pitx2 转录调控的机制了解甚少。在这里，我们使用了一种体内转基因方法来研究调节 Pitx2 转录的机制。我们鉴定了一个7kb的片段，该片段指导LacZ在口腔外胚层及其许多衍生物中的表达。对转基因胚胎的缺失分析将该片段还原为一个520 bp的区域，该区域将LacZ活性导向了Rathke的囊袋。小鼠和人类序列的比较显示保守的核因子1（NF-1）识别元件靠近共有T细胞因子（TCF）/ LEF结合位点。任一位点的突变均会消除转基因胚胎中的LacZ活性，从而确定 Pitx2 是垂体发育中Wnt信号传导的直接靶标。这些发现揭示了垂体 Pitx2 转录调节中对NF-1和TCF因子的需求，并为控制口腔外胚层及其衍生物中区域特异性转录的机制提供了见识。

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