SALL4 is directly activated by TCF/LEF in the canonical Wnt signaling pathway
SALL4 is directly activated by TCF/LEF in the canonical Wnt signaling pathway
复制标题
DOI：
10.1016/j.bbrc.2006.07.124
复制
发表时间：
2006-09-29
影响因子：
3.1
通讯作者：
Kohlhase, Juergen
中科院分区：
文献类型：
--
作者：
Boehm, Johann;Sustmann, Claudio;Kohlhase, Juergen
SALL4启动子的特征尚未确定。动物研究表明，在肢体和心脏发育过程中，SALL4位于TBX5的下游并与其相互作用，但尚未证实TBX5对SALL4的直接调节作用。对于其他SAL基因，Shh、Wnt和Fgf通路中的调节已被报道。Fgf4和Wnt3a或Wnt7a的结合可以激活鸡csall的表达。小鼠Sal11增强，但非洲爪哇Xsal2抑制典型的Wnt信号。本文介绍了SALL4启动子的克隆和功能分析。在31个碱基的最小启动子区域内，我们确定了一个共识的TCF/LEF结合位点。SALL4启动子不仅被LEF1激活，而且被TCF4E激活。Tcf/Lef结合位点突变导致启动子活性降低。我们的结果首次证明了典型的Wnt信号通路对SAL基因的直接调控。(C)2006 Elsevier Inc.保留所有权利。
The SALL4 promoter has not yet been characterized. Animal studies showed that SALL4 is downstream of and interacts with TBX5 during limb and heart development, but a direct regulation of SALL4 by TBX5 has not been demonstrated. For other SAL genes, regulation within the Shh, Wnt, and Fgf pathways has been reported. Chicken csall expression can be activated by a combination of Fgf4 and Wnt3a or Wnt7a. Murine Sal11 enhances, but Xenopus Xsal2 represses, the canonical Wnt signaling. Here we describe the cloning and functional analysis of the SALL4 promoter. Within a minimal promoter region of 31 bp, we identified a consensus TCF/LEF-binding site. The SALL4 promoter was strongly activated not only by LEF1 but also by TCF4E. Mutation of the TCF/LEF-binding site resulted in decreased promoter activation. Our results demonstrate for the first time the direct regulation of a SALL gene by the canonical Wnt signaling pathway. (c) 2006 Elsevier Inc. All rights reserved.