Xom induces proteolysis of β‐catenin through GSK3β‐mediated pathway
Abstract
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 GSK3‐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.
Document Details
- Document Type
- Pub Defense Publication
- Publication Date
- Dec 27, 2017
- Source ID
- 10.1002/1873-3468.12949
Entities
People
- Hong Gao
- Wu Bin
- Xiaoming Wu
- Yi Le
- Zhenglun Zhu
Organizations
- Harvard Medical School
- National Institutes of Health
- Tufts Medical Center
- United States Department of Defense