PUBLICATION
A beta-Catenin-Independent Dorsalization Pathway Activated by Axin/JNK Signaling and Antagonized by Aida
- Authors
- Rui, Y., Xu, Z., Xiong, B., Cao, Y., Lin, S., Zhang, M., Chan, S.C., Luo, W., Han, Y., Lu, Z., Ye, Z., Zhou, H.M., Han, J., Meng, A., and Lin, S.C.
- ID
- ZDB-PUB-070813-12
- Date
- 2007
- Source
- Developmental Cell 13(2): 268-282 (Journal)
- Registered Authors
- Meng, Anming
- Keywords
- none
- MeSH Terms
-
- Body Patterning*/drug effects
- Phenotype
- MAP Kinase Signaling System*/drug effects
- Chlorocebus aethiops
- Oligonucleotides, Antisense/pharmacology
- PubMed
- 17681137 Full text @ Dev. Cell
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 beta-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.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping