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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

Authors

  • Sanford LP
  • Ormsby I
  • Gittenberger-de Groot AC
  • Sariola H
  • Friedman R
  • Boivin GP
  • Cardell EL
  • Doetschman T

Journal

Development (Cambridge, England)

Publication Data

July 7, 1997

Associated Grants

  • Agency: NIDCD NIH HHS, Id: DC00119
  • Agency: NICHD NIH HHS, Id: HD26471
  • Agency: NHLBI NIH HHS, Id: HL41496
  • Agency: NICHD NIH HHS, Id: R01 HD026471

Mesh Terms

  • 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