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Epiboly spreads and thins the blastoderm over the yolk cell during zebrafish gastrulation.Despite of its fundamental function,little is known about the molecular mechanisms that control this coordinated cell movement.in this study,we investigated protein arginine methyltransferase 7 (Prmt7) morphants with an epibolic delay defect in zebrafish.The ratio of morphants with epiboly delay phenotypes increased as the dose of the injected morpholino (MO) increased.Here,syntenin transcripts are mateally deposited and ubiquitously expressed from the oocyte period to the early larva stage.Furthermore,we demonstrated that Prmt7 modulates epibolic movements of the enveloping layer by regulating F-actin organization.These defects can be partially rescued by re-expression of Prmt7 or syntenin protein.Analysis of the earliest cellular defects suggested a role of Prmt7 in the autonomous vegetal expansion of the yolk syncytial layer and the rearrangement of the actin cytoskeleton in extra-embryonic tissues.By a combination of knockdown studies and rescue experiments in zebrafish,we showed that epiboly relies on the molecular networking of Prmt7 by facilitating syntenin,which acts as a regulator for cytoskeleton.This study identifies the important function of the Prmt7 for the progression of zebrafish epiboly and establishes its key role in directional cell movements during early development.