期刊
GENESIS
卷 37, 期 3, 页码 139-143出版社
WILEY
DOI: 10.1002/gene.10241
关键词
Notch signaling pathway; Notch3 gene; functional redundancy
资金
- NATIONAL CANCER INSTITUTE [P30CA034196] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE [R01NS036437] Funding Source: NIH RePORTER
- NCI NIH HHS [CA34196] Funding Source: Medline
- NINDS NIH HHS [NS36437] Funding Source: Medline
The Notch signaling pathway is an evolutionarily conserved signaling mechanism and mutations in its components disrupt cell fate specification and embryonic development in many organisms. To analyze the in vivo role of the Notch3 gene in mice, we created a deletion allele by gene targeting. Embryos homozygous for this mutation developed normally and homozygous mutant adults were viable and fertile. We also examined whether we could detect genetic interactions during early embryogenesis between the Notch3 mutation and a targeted mutation of the Notch1 gene. Double homozygous mutant embryos exhibited defects normally observed in Notch1-deficient embryos, but we detected no obvious synergistic effects in the double mutants. These data demonstrate that the Notch3 gene is not essential for embryonic development or fertility in mice, and does not have a redundant function with the Notch1 gene during early embryogenesis. (C) 2003 Wiley-Liss, Inc.
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