SALL4 is directly activated by TCF/LEF in the canonical Wnt signaling pathway

被引：77
作者：
Boehm, Johann
Sustmann, Claudio
Wilhelm, Christian
Kohlhase, Juergen [1 ]
机构：
[1] Univ Freiburg, Inst Humangenet & Anthropol, Freiburg, Germany
[2] Max Planck Inst Immunobiol, Freiburg, Germany
来源：
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS | 2006年 / 348卷 / 03期
关键词：
SALL4; Okihiro syndrome; zinc finger; WNT-signaling; TCF/LEF;
D O I：
10.1016/j.bbrc.2006.07.124
中图分类号：
Q5 [生物化学]; Q7 [分子生物学];
学科分类号：
071010 ; 081704 ;
摘要：
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.
引用
收藏
页码：898 / 907
页数：10
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