The article explores the role of the Notch signaling pathway in vascular morphogenesis during embryonic development in mice. Researchers investigated the Notch4 gene, which is not essential for embryonic development but plays a partially overlapping role with Notch1 during embryogenesis. They generated Notch4-deficient mice and found that these mice were viable and fertile, but when combined with a Notch1 mutation, they exhibited severe vascular defects. This suggests that Notch1 and Notch4 have partially redundant functions in vascular development. The study also revealed that the Dll4 gene is the only Notch ligand expressed in a pattern consistent with its role in the early embryonic vasculature. This gene is essential for the Notch signaling pathway, which is crucial for vascular morphogenesis and remodeling. The Notch signaling pathway is an evolutionarily conserved mechanism that regulates cell fate specification and embryonic development in various organisms, including mammals. The findings highlight the importance of Notch signaling in regulating vascular development and homeostasis. While the Notch4 gene is not essential for embryonic development, it contributes to the functional redundancy with Notch1 during embryogenesis. The study also indicates that defects in Notch signaling can lead to severe vascular defects, as seen in the Notch1 and Notch4 double mutant embryos, which exhibited impaired angiogenic vascular remodeling. In summary, the Notch signaling pathway is essential for vascular morphogenesis and remodeling during embryonic development in mice. The Notch4 gene, while not essential for embryonic development, plays a partially overlapping role with Notch1 in this process. The study underscores the importance of Notch signaling in vascular development and provides insights into the functional redundancy between Notch1 and Notch4 genes during embryogenesis.The article explores the role of the Notch signaling pathway in vascular morphogenesis during embryonic development in mice. Researchers investigated the Notch4 gene, which is not essential for embryonic development but plays a partially overlapping role with Notch1 during embryogenesis. They generated Notch4-deficient mice and found that these mice were viable and fertile, but when combined with a Notch1 mutation, they exhibited severe vascular defects. This suggests that Notch1 and Notch4 have partially redundant functions in vascular development. The study also revealed that the Dll4 gene is the only Notch ligand expressed in a pattern consistent with its role in the early embryonic vasculature. This gene is essential for the Notch signaling pathway, which is crucial for vascular morphogenesis and remodeling. The Notch signaling pathway is an evolutionarily conserved mechanism that regulates cell fate specification and embryonic development in various organisms, including mammals. The findings highlight the importance of Notch signaling in regulating vascular development and homeostasis. While the Notch4 gene is not essential for embryonic development, it contributes to the functional redundancy with Notch1 during embryogenesis. The study also indicates that defects in Notch signaling can lead to severe vascular defects, as seen in the Notch1 and Notch4 double mutant embryos, which exhibited impaired angiogenic vascular remodeling. In summary, the Notch signaling pathway is essential for vascular morphogenesis and remodeling during embryonic development in mice. The Notch4 gene, while not essential for embryonic development, plays a partially overlapping role with Notch1 in this process. The study underscores the importance of Notch signaling in vascular development and provides insights into the functional redundancy between Notch1 and Notch4 genes during embryogenesis.