Laboratory of Genomic Systems Analysis, School of Life Sciences, University of Warwick, Coventry CV4 7AL, United Kingdom.
J Biol Chem. 2012 Feb 17;287(8):5687-97. doi: 10.1074/jbc.M111.286484. Epub 2011 Dec 13.
The expression profile of a gene is controlled by DNA sequences called cis-regulatory modules (CRMs). CRMs can function over large genomic distances and can be located many kilobases away from their target promoters. hes1 is a key developmental gene that is overexpressed in certain cancers and is a primary target of NOTCH signaling. Despite this, analysis of hes1 transcriptional control has been limited solely to its promoter. Here, we identify seven conserved DNA sequence blocks, representing the hes1 promoter and six novel CRMs, within 57 kb upstream of the mouse hes1 gene. We identify 12 binding sites for the RBP-Jκ NOTCH effector and a single M-CAT motif within these regions. We validate RBP-Jκ and TEAD family occupancy in cells in culture and test the response of each of these CRMs to active NOTCH. We show that two regions, CRM5 and CRM7, function as enhancers, and four can repress transcription. A pair of RBP-Jκ motifs arranged in a tail-tail configuration in CRM5 and the M-CAT motif in CRM7 are necessary for enhancer function. Furthermore, these enhancers are occupied by transcriptional co-activators and loop onto the hes1 promoter within the endogenous hes1 locus. This work demonstrates the power of combining computational genomics and experimental methodologies to identify novel CRMs and characterize their function.
基因的表达谱受称为顺式调控模块(CRMs)的 DNA 序列控制。CRMs 可以在很大的基因组距离上发挥作用,并且可以位于其靶启动子数千个碱基对之外。hes1 是一种在某些癌症中过度表达的关键发育基因,是 NOTCH 信号的主要靶标。尽管如此,hes1 转录控制的分析仅限于其启动子。在这里,我们在小鼠 hes1 基因上游 57kb 范围内鉴定了七个保守的 DNA 序列块,代表 hes1 启动子和六个新的 CRM。我们在这些区域中鉴定了 12 个 RBP-Jκ NOTCH 效应物的结合位点和单个 M-CAT 基序。我们验证了细胞培养中 RBP-Jκ 和 TEAD 家族的结合,并测试了这些 CRM 中每一个对活性 NOTCH 的反应。我们表明,两个区域 CRM5 和 CRM7 作为增强子起作用,而四个区域可以抑制转录。CRM5 中的 RBP-Jκ 基序以尾对尾的形式排列,CRM7 中的 M-CAT 基序是增强子功能所必需的。此外,这些增强子被转录共激活因子占据,并在体内 hes1 基因座内回环到 hes1 启动子上。这项工作证明了结合计算基因组学和实验方法来识别新的 CRM 并表征其功能的强大功能。