TGFbeta2 knockout mice have multiple developmental defects that are non-overlapping with other TGFbeta knockout phenotypes.
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.
Pubmed ID: 9217007 RIS Download
Abnormalities, Multiple | Animals | Bone and Bones | Cleft Palate | Craniofacial Abnormalities | Cyanosis | Ear, Inner | Embryonic Induction | Epithelium | Eye Abnormalities | Genes, Homeobox | Heart Defects, Congenital | Mesoderm | Mice | Mice, Inbred C57BL | Mice, Knockout | Phenotype | Transforming Growth Factor beta | Tretinoin | Urogenital Abnormalities