Abnormal lung development and cleft palate in mice lacking TGF-beta 3 indicates defects of epithelial-mesenchymal interaction.
A broad spectrum of biological activities has been proposed for transforming growth factor-beta 3 (TGF-beta 3). To study TGF-beta 3 function in development, TGF-beta 3 null mutant mice were generated by gene-targeting. Within 20 hours of birth, homozygous TGF-beta 3-/- mice die with unique and consistent phenotypic features including delayed pulmonary development and defective palatogenesis. Unlike other null mutants with cleft palate, TGF-beta 3-/- mice lack other concomitant craniofacial abnormalities. This study demonstrates an essential function for TGF-beta 3 in the normal morphogenesis of palate and lung, and directly implicates this cytokine in mechanisms of epithelial-mesenchymal interaction.
D000818:Animals; D000831:Animals, Newborn; D001483:Base Sequence; D002972:Cleft Palate / Q000196:embryology / Q000235:genetics*; D004848:Epithelium / Q000502:physiology; D008168:Lung / Q000002:abnormalities* / Q000737:chemistry / Q000196:embryology; D008648:Mesoderm / Q000502:physiology*; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D008969:Molecular Sequence Data; D009024:Morphogenesis; D010159:Palate / Q000196:embryology*; D011510:Proteolipids / Q000032:analysis; D011663:Pulmonary Surfactants / Q000032:analysis; D016212:Transforming Growth Factor beta / Q000235:genetics / Q000502:physiology*
D011510:Proteolipids; D011663:Pulmonary Surfactants; D016212:Transforming Growth Factor beta