期刊
DEVELOPMENTAL DYNAMICS
卷 236, 期 2, 页码 512-517出版社
WILEY-LISS
DOI: 10.1002/dvdy.21021
关键词
Alk2; bone morphogenetic protein; gastrulation; mouse
资金
- NHLBI NIH HHS [HL074862, R01 HL074862] Funding Source: Medline
- NIDCR NIH HHS [DE013085, R01 DE013085] Funding Source: Medline
Bone morphogenetic proteins (BMPs) have multiple functions during vertebrate development. Previously, it was shown that BMP type I receptor ALK2 (also known as ACVR1, ActR1, or ActRIA) was important for normal mouse gastrulation by deleting exon 4 or exon 5 of AM. 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 (Delta 5/Delta 5)) and embryos with an exon 7 deletion (Alk2 (Delta 7/Delta 7)). Both Alk2(Delta 5/Delta 5) and Alk2(Delta 7/Delta 7) mutants showed identical morphological gastrulation defects. Histological examinations and molecular marker analyses revealed identical abnormal gastrulation phenotypes in Alk2(Delta 5/Delta 5) and Alk2(Delta 7/Delta 7) mutants. Although FgfS was expressed in the primitive streak of Alk2(Delta 5/Delta 5) and Alk2 (Delta 7/Delta 7) mutants, Brachyury, Wnt3a, and Tbx6 were dramatically downregulated in Alk2 (Delta 5/Delta 5) and Alk2(Delta 7/Delta 7) 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.
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