Blood vessel development is a complex but orderly process that is tightly regulated.A number of secreted factors produced by surrounding cells regulate endothelial cell(EC)differentiation,proliferation,and migration.The epidermal growth factor(EGF)repeat usually comprises a sequence around 45 amino acid residues and three disulfide bridges.The EGF repeat motif defines a superfamily of diverse protein involved in regulating a variety of cellular and physiological processes,such as cell cycle,cell adhesion,proliferation,migration,and neural development.Here we report a somite-secreted EGF protein,MAE,regulates zebrafish embryonic angiogenesis.It was demonstrated that MAE was expressed in zebrafish developing somite during a time window encompassing many key steps in embryonic angiogenesis.Loss of MAE function in zebrafish embryos specifically interrupts branching angiogenesis of intersegmental vessels(ISVs).ISVs in MAE morphants grew only halfway through their ventral trajectory and stalled at the boundary between the notochord and neural tube,accompanied with the cell number reduction of ISV.Furthermore,we proved that the filopodia number of ISV tip cells was significantly reduced in MAE morphants.These phenotypes are reminiscent of Notch overexpression.In addition,our results show that Loss of MAE function resulted in up-regulation of Notch signaling.And inhibition of Notch signal could rescue the angiogenesis defects phenotypes of MAE morphants.