ZFIN ID: ZDB-PUB-961014-226
Active complex formation of type I and type II activin and TGF beta receptors in vivo as studied by overexpression in zebrafish embryos
DeVries, C.J.M., DeBoer, J., Joore, J., Strähle, U., VanAchterberg, T.A.E., Huylebröck, D., Verschüren, K., Miyazono, K., VandenEijnden-vanRaaij, A.J.M., and Zivkovic, D.
Date: 1996
Source: Mechanisms of Development   54(2): 225-236 (Journal)
Registered Authors: Jongejan-Zivkovic, Dana, Joore, Jos, Strähle, Uwe
Keywords: none
MeSH Terms:
  • Activins
  • Animals
  • Base Sequence
  • Inhibins/genetics
  • Inhibins/metabolism*
  • Mesoderm
  • Mice
  • Molecular Sequence Data
  • Oligodeoxyribonucleotides
  • Protein Binding
  • Protein-Serine-Threonine Kinases/metabolism
  • RNA/administration & dosage
  • Receptors, Transforming Growth Factor beta/genetics
  • Receptors, Transforming Growth Factor beta/metabolism*
  • Zebrafish/embryology*
  • Zebrafish/genetics
PubMed: 8652415 Full text @ Mech. Dev.
We have investigated the involvement of activin receptors and TGF beta type I receptor in zebrafish development. Overexpression of either full-length or a truncated form of mouse ActR-IIA interferes with the development. Different splice variants of mouse ActR-IIB have distinct effects; ActR- IIB4 induces abnormal embryos, whereas ActR-IIB2 does not. Activin and TGF beta type I receptors can induce axis duplications. Co-expression of ActR-IA or ActR-IB with the type II activin receptors results in a synergistic increase of the frequency of axis duplication. Moreover, ActR-IIB2 is synergistic with ActR-IA and ActR-IB, demonstrating that ActR- IIB2 can interact with the zebrafish ligand. Overexpression of TGF beta R-I with ActR-IIA or ActR IIB4 results in a synergistic increase in frequency of abnormal embryos, whereas in combination with ActR-IIB2 no such increase occurs.