Xenopus skip modulates Wnt/β-catenin signaling and functions in neural crest induction

Ying Wang, Yu Fu, Lei Gao, Guixin Zhu, Juan Liang, Chan Gao, Binlu Huang, Ursula Fenger, Christof Niehrs, Ye Guang Chen, Wei Wu*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

32 Citations (Scopus)

Abstract

The β-catenin-lymphoid enhancer factor (LEF) protein complex is the key mediator of canonical Wnt signaling and initiates target gene transcription upon ligand stimulation. In addition to β-catenin and LEF themselves, many other proteins have been identified as necessary cofactors. Here we report that the evolutionally conserved splicing factor and transcriptional co-regulator, SKIP/SNW/NcoA62, forms a ternary complex with LEF1 and HDAC1 and mediates the repression of target genes. Lossof-function studies showed that SKIP is obligatory for Wnt signaling-induced target gene transactivation, suggesting an important role of SKIP in the canonical Wnt signaling. Consistent with its involvement in β-catenin signaling, the C-terminally truncated forms of SKIP are able to stabilize β-catenin and enhance Wnt signaling. In Xenopus embryos, both overexpression and knockdown of Skip lead to reduced neural crest induction, consistent with down-regulated Wnt signaling in both cases. Our results indicate that SKIP is a novel component of the β-catenin transcriptional complex.

Original languageEnglish
Pages (from-to)10890-10901
Number of pages12
JournalJournal of Biological Chemistry
Volume285
Issue number14
DOIs
Publication statusPublished - 2 Apr 2010
Externally publishedYes

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