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Xom induces proteolysis of β‐catenin through GSK 3β‐mediated pathway
Author(s) -
Wu Bin,
Gao Hong,
Le Yi,
Wu Xiaoming,
Zhu Zhenglun
Publication year - 2018
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1002/1873-3468.12949
Subject(s) - proteolysis , microbiology and biotechnology , catenin , ubiquitin , phosphorylation , signal transduction , biology , chemistry , biochemistry , wnt signaling pathway , enzyme , gene
The dorsal cell fate determination factor β‐catenin and its antagonist, the ventral cell fate determination factor Xom, are expressed and distributed in a polarized fashion during early vertebrate embryogenesis. Ubiquitin‐mediated proteolysis has been shown to control the abundance of both β‐catenin and Xom. However, the mechanism of ubiquitin‐mediated proteolysis in regulating dorsoventral patterning remains largely unclear. Our current study shows that Xom induces proteolysis of β‐catenin through GSK 3‐mediated phosphorylation of Ser33/37 of β‐catenin. Our findings reveal a novel pathway that regulates β‐catenin stability, and suggest, for the first time, a critical function of ubiquitin‐mediated proteolysis in balancing the integration of dorsal–ventral signals and the polarized distribution of β‐catenin and Xom during dorsoventral axis formation.