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Churchill and Sip1a repress fibroblast growth factor signaling during zebrafish somitogenesis
Author(s) -
Kok Fatma O.,
Shepherd Iain T.,
Sirotkin Howard I.
Publication year - 2010
Publication title -
developmental dynamics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.634
H-Index - 141
eISSN - 1097-0177
pISSN - 1058-8388
DOI - 10.1002/dvdy.22201
Subject(s) - somitogenesis , biology , fgf8 , somite , fibroblast growth factor , zebrafish , morpholino , microbiology and biotechnology , gastrulation , mesoderm , signal transduction , embryo , genetics , gene , receptor , embryonic stem cell , embryogenesis
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. Developmental Dynamics 239:548–558, 2010. © 2009 Wiley‐Liss, Inc.