Open AccessTGFβ2 knockout mice have multiple developmental defects that are non-overlapping with other TGFβ knockout phenotypes
Author(s) -
Lynn Sanford,
Ilona Ormsby,
Adriana C. Gittenbergerde Groot,
Hannu Sariola,
Rick A. Friedman,
Greg P. Boivin,
Emma Lou Cardell,
Thomas Doetschman
Publication year - 1997
Publication title -
development
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.754
H-Index - 325
eISSN - 1477-9129
pISSN - 0950-1991
DOI - 10.1242/dev.124.13.2659
Subject(s) - biology , neural crest , conditional gene knockout , transforming growth factor , knockout mouse , phenotype , mesenchyme , microbiology and biotechnology , transforming growth factor beta , gene knockout , extracellular matrix , mesenchymal stem cell , genetics , gene , embryo
The growth and differentiation factor transforming growth factor-beta2 (TGFbeta2) is thought to play important roles in multiple developmental processes. Targeted disruption of the TGFbeta2 gene was undertaken to determine its essential role in vivo. TGFbeta2-null mice exhibit perinatal mortality and a wide range of developmental defects for a single gene disruption. These include cardiac, lung, craniofacial, limb, spinal column, eye, inner ear and urogenital defects. The developmental processes most commonly involved in the affected tissues include epithelial-mesenchymal interactions, cell growth, extracellular matrix production and tissue remodeling. In addition, many affected tissues have neural crest-derived components and simulate neural crest deficiencies. There is no phenotypic overlap with TGFbeta1- and TGFbeta3-null mice indicating numerous non-compensated functions between the TGFbeta isoforms.