XTcf-3 transcription factor mediates beta-catenin-induced axis formation in Xenopus embryos
XTcf-3 transcription factor mediates beta-catenin-induced axis formation in Xenopus embryos
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DOI：
10.1016/s0092-8674(00)80112-9
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发表时间：
1996-08-09
期刊：
影响因子：
64.5
通讯作者：
Clevers, H
中科院分区：
文献类型：
--
作者：
Molenaar, M;vandeWetering, M;Clevers, H
XTcf-3是母系表达的爪蟾HMG盒因子Tcf-1和lef1的同源物。XTcf-3的n端结合β -连环蛋白。胚胎中微量注射xtcf - 3mrna导致β -连环蛋白的核易位。β -catenin-XTcf-3复合物在瞬时报告基因试验中激活转录，而XTcf-3本身是沉默的。XTcf-3 （δ N）的N端缺失取消了与β -连环蛋白的相互作用，以及随之而来的转录激活。这种显性阴性突变体抑制了微注射Delta-连环蛋白诱导的轴复制。注射到4细胞期胚胎的背面卵裂球后，它也抑制内源性轴规范。我们提出β -连环蛋白的信号传导涉及与XTcf-3形成复合物，随后是核易位和特定XTcf-3靶基因的激活。
XTcf-3 is a maternally expressed Xenopus homolog of the mammalian HMG box factors Tcf-1 and Lef-1 The N-terminus of XTcf-3 binds to beta-catenin. Microinjection of XTcf-3 mRNA in embryos results in nuclear translocation of beta-catenin. The beta-catenin-XTcf-3 complex activates transcription in a transient reporter gene assay, while XTcf-3 by itself is silent. N-terminal deletion of XTcf-3 (Delta N) abrogates the interaction with beta-catenin, as well as the consequent transcription activation. This dominant-negative Delta N mutant suppresses the induction of axis duplication by microinjected Delta-catenin. It also suppresses endogenous axis specification upon injection into the dorsal blastomeres of a 4-cell-stage embryo. We propose that signaling by beta-catenin involves complex formation with XTcf-3, followed by nuclear translocation and activation of specific XTcf-3 target genes.