Epiboly spreads and thins the blastoderm over the yolk cell during zebrafish gastrulation.Although recent studies have begun to elucidate the processes that underlie these epibolic movements,the cellular and molecular mechanisms involved remain to be fully defined.During early development,zygotic genome undergo dramatic epigenetic alterations.Histone modification enzymes may be important factors that contribute to the changes.In this study,we show that knockdown of Protein arginine methyltransferase7(PRMT7)by antisense morpholino oligo(AMO)resulted in delayed epiboly,subsequent developmental defects,and phenocopying E-cadherin mutants in a dose-dependent manner.There are hypermethylation of H4R3me2s in epiboly initation and reduced levels of H4R3me2s in the AMO-injected morphants.