This article is a US Government work and, as such, is in the public domain in the United States of America.
Patterns & Phenotypes
BMP type I receptor ALK2 is essential for proper patterning at late gastrulation during mouse embryogenesis†
Version of Record online: 20 NOV 2006
Published 2006 Wiley-Liss, Inc.
Volume 236, Issue 2, pages 512–517, February 2007
How to Cite
Komatsu, Y., Scott, G., Nagy, A., Kaartinen, V. and Mishina, Y. (2007), BMP type I receptor ALK2 is essential for proper patterning at late gastrulation during mouse embryogenesis. Dev. Dyn., 236: 512–517. doi: 10.1002/dvdy.21021
- Issue online: 10 JAN 2007
- Version of Record online: 20 NOV 2006
- Manuscript Accepted: 18 OCT 2006
- NIH. Grant Numbers: HL074862, DE013085
- Intramural Research Program of the National Institutes of Health
- National Institute of Environmental Health Sciences (NIH/NIEHS)
- bone morphogenetic protein;
Bone morphogenetic proteins (BMPs) have multiple functions during vertebrate development. Previously, it was shown that BMP type I receptor ALK2 (also known as ACVRI, ActRI, or ActRIA) was important for normal mouse gastrulation by deleting exon 4 or exon 5 of Alk2. Recently, flanking exon 7 by loxP sites generated a conditional allele for Alk2. To assess whether the deletion of exon 7 causes functional null of ALK2, and does not produce a dominant negative form or a partially functional form of ALK2, we performed a comparative analysis between Alk2 homozygous mutant embryos with an exon 5 deletion (Alk2Δ5/Δ5) and embryos with an exon 7 deletion (Alk2Δ7/Δ7). Both Alk2Δ5/Δ5 and Alk2Δ7/Δ7 mutants showed identical morphological gastrulation defects. Histological examinations and molecular marker analyses revealed identical abnormal gastrulation phenotypes in Alk2Δ5/Δ5 and Alk2Δ7/Δ7 mutants. Although Fgf8 was expressed in the primitive streak of Alk2Δ5/Δ5 and Alk2Δ7/Δ7 mutants, Brachyury, Wnt3a, and Tbx6 were dramatically downregulated in Alk2Δ5/Δ5 and Alk2Δ7/Δ7 mutants. These results indicate that deletion of exon 7 for Alk2 leads to a functionally null mutation in vivo, and Alk2 is crucial for sustaining the proper gastrulation events in early mouse embryogenesis. Developmental Dynamics 236:512–517, 2007. Published 2006 Wiley-Liss, Inc.