Mice deficient for BMP2 are nonviable and have defects in amnion/chorion and cardiac development

TLDR

BMP2 is expressed in extraembryonic mesoderm cells and promyocardium, indicating its importance in early embryonic and extraembryonic development. The study sought to elucidate BMP2’s function in mammalian development by generating mice lacking the mature BMP2 region. A targeted deletion of the Bmp2 mature region was introduced into embryonic stem cells to create knockout mice. Homozygous BMP2 deletion caused embryonic lethality, failed proamniotic canal closure resulting in amnion/chorion malformations, and cardiac defects in the exocoelomic cavity, demonstrating BMP2’s essential role in extraembryonic and embryonic development.

Abstract

ABSTRACT 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.