PUBLICATION

Def6 Is Required for Convergent Extension Movements during Zebrafish Gastrulation Downstream of Wnt5b Signaling

Authors
Goudevenou, K., Martin, P., Yeh, Y.J., Jones, P., and Sablitzky, F.
ID
ZDB-PUB-111115-2
Date
2011
Source
PLoS One   6(10): e26548 (Journal)
Registered Authors
Martin, Paul
Keywords
none
MeSH Terms
  • Animals
  • Base Sequence
  • Gastrulation*
  • Gene Knockdown Techniques
  • Humans
  • In Situ Hybridization
  • Mice
  • Oligonucleotides
  • Signal Transduction*
  • Wnt Proteins/genetics
  • Wnt Proteins/metabolism*
  • Zebrafish/embryology*
  • Zebrafish Proteins/genetics
  • Zebrafish Proteins/metabolism*
PubMed
22039507 Full text @ PLoS One
Abstract
During gastrulation, convergent extension (CE) cell movements are regulated through the non-canonical Wnt signaling pathway. Wnt signaling results in downstream activation of Rho GTPases that in turn regulate actin cytoskeleton rearrangements essential for co-ordinated CE cell movement. Rho GTPases are bi-molecular switches that are inactive in their GDP-bound stage but can be activated to bind GTP through guanine nucleotide exchange factors (GEFs). Here we show that def6, a novel GEF, regulates CE cell movement during zebrafish gastrulation. Def6 morphants exhibit broadened and shortened body axis with normal cell fate specification, reminiscent of the zebrafish mutants silberblick and pipetail that lack Wnt11 or Wnt5b, respectively. Indeed, def6 morphants phenocopy Wnt5b mutants and ectopic overexpression of def6 essentially rescues Wnt5b morphants, indicating a novel role for def6 as a central GEF downstream of Wnt5b signaling. In addition, by knocking down both def6 and Wnt11, we show that def6 synergises with the Wnt11 signaling pathway.
Genes / Markers
Figures
Show all Figures
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping