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.
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
Figures
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping