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The Notch gene family encodes large transmembrane receptors that are components of an evolutionarily conserved intercellular signaling mechanism. To assess the role of the  Notch4  gene, we generated Notch4 -deficient mice by gene targeting. Embryos homozygous for this mutation developed normally, and homozygous mutant adults were viable and fertile. However, the  Notch4  mutation displayed genetic interactions with a targeted mutation of the related Notch1  gene. Embryos homozygous for mutations of both the Notch4  and  Notch1  genes often displayed a more severe phenotype than  Notch1  homozygous mutant embryos. Both Notch1  mutant and  Notch1/Notch4  double mutant embryos displayed severe defects in angiogenic vascular remodeling. Analysis of the expression patterns of genes encoding ligands for Notch family receptors indicated that only the  Dll4 gene is expressed in a pattern consistent with that expected for a gene encoding a ligand for the  Notch1  and  Notch4  receptors in the early embryonic vasculature. These results reveal an essential role for the Notch signaling pathway in regulating embryonic vascular morphogenesis and remodeling, and indicate that whereas the Notch4  gene is not essential during embryonic development, the Notch4  and  Notch1  genes have partially overlapping roles during embryogenesis in mice.

Notch signaling is essential for vascular morphogenesis in mice