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Dual specificity of activin type II receptor ActRIIb in dorso‐ventral patterning during zebrafish embryogenesis
Author(s) -
Nagaso Hideyuki,
Suzuki Atsushi,
Tada Masazumi,
Ueno Naoto
Publication year - 1999
Publication title -
development, growth and differentiation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.864
H-Index - 66
eISSN - 1440-169X
pISSN - 0012-1592
DOI - 10.1046/j.1440-169x.1999.00418.x
Subject(s) - zebrafish , activin receptor , biology , activin type 2 receptors , mesoderm , acvr2b , microbiology and biotechnology , bone morphogenetic protein , nodal signaling , bmpr2 , blastula , embryo , embryogenesis , receptor , tgf beta signaling pathway , signal transduction , transforming growth factor , gastrulation , embryonic stem cell , genetics , gene
Members of the transforming growth factor‐β (TGF‐β) superfamily are thought to regulate specification of a variety of tissue types in early embryogenesis. These effects are mediated through a cell surface receptor complex, consisting of two classes of ser/thr kinase receptor, type I and type II. In the present study, cDNA encoding zebrafish activin type II receptors, ActRIIa and ActRIIb was cloned and characterized. Overexpression of ActRIIb in zebrafish embryos caused dorsalization of embryos, as observed in activin‐overexpressing embryos. However, in blastula stage embryos, ActRIIb induced formation of both dorsal and ventro‐lateral mesoderm. It has been suggested that these inducing signals from ActRIIb are mediated through each specific type I receptor, TARAM‐A and BMPRIA, depending on activin and bone morphogenetic protein (BMP), respectively. In addition, it was shown that a kinase‐deleted form of ActRIIb (dnActRIIb) suppressed both activin‐ and BMP‐like signaling pathways. These results suggest that ActRIIb at least has dual roles in both activin and BMP signaling pathways during zebrafish embryogenesis.