Mice deficient for BMP2 are nonviable and have defects in amnion/chorion and cardiac development.
To address the function of bone morphogenetic protein-2 (BMP2) in mammalian development, mice with a targeted deletion of the Bmp2 mature region were generated using embryonic stem cell technology. This mutation caused embryonic lethality when homozygous. Mutant embryos failed to close the proamniotic canal, which caused the malformation of the amnion/chorion. BMP2-deficient embryos also exhibited a defect in cardiac development, manifested by the abnormal development of the heart in the exocoelomic cavity. These defects are consistent with the expression of Bmp2 in the extraembryonic mesoderm cells and promyocardium. Thus BMP2 is a critical factor for both extraembryonic and embryonic development.
Zhang
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H
Department of Molecular and Human Genetics, Baylor College of Medicine, Houston, Texas 77030, USA.
Bradley
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A
D000482:Allantois / Q000196:embryology; D000650:Amnion / Q000196:embryology; D000818:Animals; D055396:Bone Morphogenetic Protein 2; D019485:Bone Morphogenetic Proteins / Q000235:genetics / Q000502:physiology*; D002823:Chorion / Q000196:embryology; D005260:Female; D017353:Gene Deletion; D015870:Gene Expression; D006321:Heart / Q000196:embryology*; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D016212:Transforming Growth Factor beta
C525719:Bmp2 protein, mouse; D055396:Bone Morphogenetic Protein 2; D019485:Bone Morphogenetic Proteins; D016212:Transforming Growth Factor beta