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Expression of the inhibitory Smad7 in early mouse development and upregulation during embryonic vasculogenesis
Author(s) -
Zwijsen An,
Van Rooijen Marga A.,
Goumans Marie–José,
Dewulf Nathalie,
Bosman Erika A.,
Ten Dijke Peter,
Mummery Christine L.,
Huylebroeck Danny
Publication year - 2000
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 - 10.1002/1097-0177(200008)218:4<663::aid-dvdy1020>3.0.co;2-7
Subject(s) - biology , smad , microbiology and biotechnology , embryonic stem cell , receptor , gastrulation , in situ hybridization , transforming growth factor , zygote , embryo , embryogenesis , gene expression , gene , genetics
SMAD proteins are downstream targets of serine/threonine kinase receptors of the transforming growth factor β (TGFβ) superfamily. Ligands activating these receptors regulate cell growth, differentiation and development in many tissues of various organisms. In mammals eight different Smad genes are known, each with different roles in mediating signalling between plasma membrane and nucleus. Smad6 and Smad7 are inhibitors of TGFβ family signalling. They are both expressed in human adult vascular endothelial cells, particularly after these cells have been subjected to shear stress (Topper et al. [1997] Proc Natl Acad Sci USA 94:9314–9319). Here we show by reverse transcriptase polymerase chain reaction and in situ hybridization that Smad 7 mRNA is highly expressed in the developing vascular system of the mouse embryo but is also detectable much earlier in preimplantation embryos and during gastrulation. We also demonstrate by transient transgenesis that overexpression of Smad 7 in mouse zygotes inhibits development beyond the 2‐cell stage. This confirms earlier conclusions of similar, but complementary, experiments using a dominant negative type II TGFβ receptor demonstrating that TGFβ signalling is required for normal preimplantation development. © 2000 Wiley‐Liss, Inc.