Terasaki Harumi, Murakami Ryohei, Yasuhiko Yukuto, Shin-I Tadasu, Kohara Yuji, Saga Yumiko, Takeda Hiroyuki
Graduate School of Science, University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-0033, Japan.
Dev Growth Differ. 2006 Apr;48(3):153-68. doi: 10.1111/j.1440-169X.2006.00853.x.
Somitogenesis is a critical step during the formation of metameric structures in vertebrates. Recent studies in mouse, chick, zebrafish and Xenopus have revealed that several factors, such as T-box genes, Notch/Delta, Wnt, retinoic acid and FGF signaling, are involved in the specification of nascent somites. By interacting with these pathways, the Mesp2-like bHLH transcription factors are transiently expressed in the anterior presomitic mesoderm and play a crucial role in somite formation. The regulatory mechanisms of Mesp2 and its related genes during somitogenesis have been studied in mouse and Xenopus. However, the precise mechanism that regulates the transcriptional activity of Mesp2 has yet to be determined. In our current report, we identify the essential enhancer element of medaka mesp-b, an orthologue of mouse Mesp2, using transgenic techniques and embryo manipulation. Our results demonstrate that a region of approximately 2.8 kb, upstream of the mesp-b gene, is responsible for both the initiation and anterior localization of mesp-b transcription within a somite primordium. Furthermore, putative motifs for both T-box transcription factors and Notch/Delta signaling are present in this enhancer region and are essential for activity.
体节发生是脊椎动物分节结构形成过程中的关键步骤。最近在小鼠、鸡、斑马鱼和非洲爪蟾中的研究表明，几种因子，如T盒基因、Notch/Delta、Wnt、视黄酸和FGF信号通路，参与了新生体节的特化。通过与这些信号通路相互作用，Mesp2样bHLH转录因子在前体节中胚层中短暂表达，并在体节形成中起关键作用。在小鼠和非洲爪蟾中已经研究了Mesp2及其相关基因在体节发生过程中的调控机制。然而，调节Mesp2转录活性的精确机制尚未确定。在我们当前的报告中，我们利用转基因技术和胚胎操作鉴定了青鳉mesp-b（小鼠Mesp2的同源物）的必需增强子元件。我们的结果表明，mesp-b基因上游约2.8 kb的区域负责体节原基内mesp-b转录的起始和前部定位。此外，该增强子区域中存在T盒转录因子和Notch/Delta信号通路的假定基序，并且这些基序对于活性至关重要。
