ZFIN ID: ZDB-PUB-100105-17
Churchill and Sip1a repress fibroblast growth factor signaling during zebrafish somitogenesis
Kok, F.O., Shepherd, I.T., and Sirotkin, H.I.
Date: 2010
Source: Developmental dynamics : an official publication of the American Association of Anatomists   239(2): 548-558 (Journal)
Registered Authors: Shepherd, Iain T., Sirotkin, Howard
Keywords: Churchill, Sip1, FGF, somitogenesis, zebrafish
MeSH Terms:
  • Animals
  • Biological Clocks*
  • Fibroblast Growth Factors/metabolism*
  • Gene Expression Regulation, Developmental
  • Gene Knockdown Techniques
  • Mesoderm/metabolism*
  • Repressor Proteins/genetics
  • Repressor Proteins/metabolism*
  • Signal Transduction
  • Trans-Activators/genetics
  • Trans-Activators/metabolism*
  • Zebrafish
  • Zebrafish Proteins/genetics
  • Zebrafish Proteins/metabolism*
PubMed: 20034103 Full text @ Dev. Dyn.
Cell-type specific regulation of a small number of growth factor signal transduction pathways generates diverse developmental outcomes. The zinc finger protein Churchill (ChCh) is a key effector of fibroblast growth factor (FGF) signaling during gastrulation. ChCh is largely thought to act by inducing expression of the multifunctional Sip1 (Smad Interacting Protein 1). We investigated the function of ChCh and Sip1a during zebrafish somitogenesis. Knockdown of ChCh or Sip1a results in misshapen somites that are short and narrow. As in wild-type embryos, cycling gene expression occurs in the developing somites in ChCh and Sip1a compromised embryos, but expression of her1 and her7 is maintained in formed somites. In addition, tail bud fgf8 expression is expanded anteriorly in these embryos. Finally, we found that blocking FGF8 restores somite morphology in ChCh and Sip1a compromised embryos. These results demonstrate a novel role for ChCh and Sip1a in repression of FGF activity.