A β-Catenin-Independent Dorsalization Pathway Activated by Axin/JNK Signaling and Antagonized by Aida

Yanning Rui, Zhen Xu, Bo Xiong, Ying Cao, Shuyong Lin, Min Zhang, Siu Chiu Chan, Wen Luo, Ying Han, Zailian Lu, Zhiyun Ye, Hai Meng Zhou, Jiahuai Han, Anming Meng, Sheng Cai Lin

Research output: Contribution to journalArticlepeer-review

38 Scopus citations

Abstract

Axin is a scaffold protein that controls multiple important pathways, including the canonical Wnt pathway and JNK signaling. Here we have identified an Axin-interacting protein, Aida, which blocks Axin-mediated JNK activation by disrupting Axin homodimerization. During investigation of in vivo functions of Axin/JNK signaling and aida in development, it was found that Axin, besides ventralizing activity by facilitating β-catenin degradation, possesses a dorsalizing activity that is mediated by Axin-induced JNK activation. This dorsalizing activity is repressed when aida is overexpressed in zebrafish embryos. Whereas Aida-MO injection leads to dorsalized embryos, JNK-MO and MKK4-MO can ventralize embryos. The anti-dorsalization activity of aida is conferred by its ability to block Axin-mediated JNK activity. We further demonstrate that dorsoventral patterning regulated by Axin/JNK signaling is independent of maternal or zygotic Wnt signaling. We have thus identified a dorsalization pathway that is exerted by Axin/JNK signaling and its inhibitor Aida during vertebrate embryogenesis.

Original languageEnglish (US)
Pages (from-to)268-282
Number of pages15
JournalDevelopmental Cell
Volume13
Issue number2
DOIs
StatePublished - Aug 7 2007

Bibliographical note

Funding Information:
We thank Dr. T. Hirano (Osaka University, Japan) for the zebrafish Axin cDNA and Dr. D.M. Virshup for comments. This work was supported by grants from National Science Foundation (30528014, to S.C.L), National Basic Research Program of China (2006CB503900, to S.C.L; 2006CB943401 and 2005CB522502, to A.M.M.), the Fujian and Xiamen Councils of Science and Technology (2002F002 and 20055004, to S.C.L.), and the Hong Kong Research Grants Council (6416/05M, to S.C.L.).

Keywords

  • DEVBIO
  • SIGNALING

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