| First Author | Komatsu Y | Year | 2007 |
| Journal | Dev Dyn | Volume | 236 |
| Issue | 2 | Pages | 512-7 |
| PubMed ID | 17117439 | Mgi Jnum | J:117234 |
| Mgi Id | MGI:3695845 | Doi | 10.1002/dvdy.21021 |
| Citation | Komatsu Y, et al. (2007) BMP type I receptor ALK2 is essential for proper patterning at late gastrulation during mouse embryogenesis. Dev Dyn 236(2):512-7 |
| abstractText | 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 (Alk2(Delta5/Delta5)) and embryos with an exon 7 deletion (Alk2(Delta7/Delta7)). Both Alk2(Delta5/Delta5) and Alk2(Delta7/Delta7) mutants showed identical morphological gastrulation defects. Histological examinations and molecular marker analyses revealed identical abnormal gastrulation phenotypes in Alk2(Delta5/Delta5) and Alk2(Delta7/Delta7) mutants. Although Fgf8 was expressed in the primitive streak of Alk2(Delta5/Delta5) and Alk2(Delta7/Delta7) mutants, Brachyury, Wnt3a, and Tbx6 were dramatically downregulated in Alk2(Delta5/Delta5) and Alk2(Delta7/Delta7) 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. |
