PUBLICATION
Wnt-5/pipetail functions in vertebrate axis formation as a negative regulator of Wnt/{beta}-catenin activity
- Authors
- Westfall, T.A., Brimeyer, R., Twedt, J., Gladon, J., Olberding, A., Furutani-Seiki, M., and Slusarski, D.C.
- ID
- ZDB-PUB-030908-6
- Date
- 2003
- Source
- The Journal of cell biology 162(5): 889-898 (Journal)
- Registered Authors
- Furutani-Seiki, Makoto, Slusarski, Diane C.
- Keywords
- none
- MeSH Terms
-
- Animals
- Body Patterning*
- Calcium/metabolism
- Calcium-Calmodulin-Dependent Protein Kinase Type 2
- Calcium-Calmodulin-Dependent Protein Kinases/metabolism
- Cytoskeletal Proteins/metabolism*
- Female
- Glycoproteins/metabolism*
- Homeodomain Proteins/genetics
- Homeodomain Proteins/metabolism
- In Situ Hybridization
- Mitogens/metabolism*
- Morphogenesis
- Phenotype
- Proto-Oncogene Proteins/genetics
- Proto-Oncogene Proteins/metabolism*
- Signal Transduction/physiology
- Trans-Activators/metabolism*
- Wnt Proteins
- Zebrafish/anatomy & histology
- Zebrafish/embryology*
- Zebrafish/physiology
- Zebrafish Proteins/genetics
- Zebrafish Proteins/metabolism*
- beta Catenin
- PubMed
- 12952939 Full text @ J. Cell Biol.
Citation
Westfall, T.A., Brimeyer, R., Twedt, J., Gladon, J., Olberding, A., Furutani-Seiki, M., and Slusarski, D.C. (2003) Wnt-5/pipetail functions in vertebrate axis formation as a negative regulator of Wnt/{beta}-catenin activity. The Journal of cell biology. 162(5):889-898.
Abstract
We provide genetic evidence defining a role for noncanonical Wnt function in vertebrate axis formation. In zebrafish, misexpression of Wnt-4, -5, and -11 stimulates calcium (Ca2+) release, defining the Wnt/Ca2+ class. We describe genetic interaction between two Wnt/Ca2+ members, Wnt-5 (pipetail) and Wnt-11 (silberblick), and a reduction of Ca2+ release in Wnt-5/pipetail. Embryos genetically depleted of both maternal and zygotic Wnt-5 product exhibit cell movement defects as well as hyperdorsalization and axis-duplication phenotypes. The dorsalized phenotypes result from increased beta-catenin accumulation and activation of downstream genes. The Wnt-5 loss-of-function defect is consistent with Ca2+ modulation having an antagonistic interaction with Wnt/beta-catenin signaling.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping