Conserved and divergent coordination between ZGA and histone modifications in porcine, mouse, and human early embryos. Broad H3K4me3 domains are already established at ZGA gene promoters in mouse oocytes, which are inherited upon fertilization and are reshaped into sharp peaks during mouse ZGA (two-cell stage). In contrast, porcine and human oocytes contain sharp H3K4me3 peaks at their ZGA gene promoters. Notably, de novo H3K4me3 establishment is observed at these promoters upon fertilization, resulting in H3K4me3 peaks spreading to form broad domains in pre-ZGA embryos (pig: one- to two-cell stages; human: four-cell stage). Nevertheless, these broad domains are reshaped into sharp form again during porcine and human ZGA (pig: four-cell stage; human: eight-cell stage), and H3K4me3 modification maintains sharp form after ZGA among the three species. For H3K27me3 modification, ZGA gene promoters exhibit weak H3K27me3 signal in mouse oocytes and fertilized embryos at all pre-implantation stages. These gene promoters also exhibit weak H3K27me3 signal in porcine oocytes and fertilized embryos at the two- to eight-cell stages but exhibit strong H3K27me3 signal in human oocytes and pre-ZGA embryos. More importantly, de novo H3K27me3 establishment is observed at ZGA gene promoters after porcine and human ZGA, resulting in promoter bivalency establishment (H3K4me3 and H3K27me3 colocalization) in their post-ZGA embryos.
