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First published online 30 August 2006
doi: 10.1242/dev.02552
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1 Laboratory of Reproductive and Developmental Toxicology, National Institute of
Environmental Health Sciences, 111 T. W. Alexander Drive, PO Box 12233, MD
C4-10, C458, Research Triangle Park, NC 27709, USA.
2 Department of Cell Biology, Duke University Medical Center, Durham NC 27710,
USA.
* Author for correspondence (e-mail: mishina{at}niehs.nih.gov)
Accepted 26 July 2006
Bmpr1a encodes the BMP type IA receptor for bone morphogenetic proteins (BMPs), including 2 and 4. Here, we use mosaic inactivation of Bmpr1a in the epiblast of the mouse embryo (Bmpr-MORE embryos) to assess functions of this gene in mesoderm development. Unlike Bmpr1a-null embryos, which fail to gastrulate, Bmpr-MORE embryos initiate gastrulation, but the recruitment of prospective paraxial mesoderm cells to the primitive streak is delayed. This delay causes a more proximal distribution of cells with paraxial mesoderm character within the primitive streak, resulting in a lateral expansion of somitic mesoderm to form multiple columns. Inhibition of FGF signaling restores the normal timing of recruitment of prospective paraxial mesoderm and partially rescues the development of somites. This suggests that BMP and FGF signaling function antagonistically during paraxial mesoderm development.
Key words: Epiblast, Primitive streak, Paraxial mesoderm, Somites, BMP, FGF, Mouse
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