GSE98151
Reprogramming of H3K9me3-dependent heterochromatin during mammalian early embryo development [WGBS]
H3K9me3-dependent heterochromatin is considered as one of the major barriers for cell fate changes, and must be reprogrammed during fertilization to reactivate highly specialized paternal and maternal genome to establish totipotency. However, the molecular details are lacked for early embryos due to the limited materials. Here we map the genome-wide distribution of H3K9me3 modification in the early embryo as well as in the cell fate determined embryonic tissues after implantation. We find that H3K9me3 exhibits distinct dynamic features in promoters and retro-transposons. Both maternal and paternal genome undergo large scale of H3K9me3 reestablishment after fertilization, and the imbalance of maternal H3K9me3 signal over paternal last until the blastocyst stage. The rebuilding of H3K9me3 on LTR retro-transposons maintains its repression state after the global DNA demethylation, and we further discover that Chaf1a is essential for the establishment of H3K9me3 on LTRs and the loss function of Chaf1a leads to embryo development failure. Finally, we find that lineage specific H3K9me3 is established after lineage commitment in post-implantation embryos. Thus, our data demonstrate that H3K9me3-dependent heterochromatin undergoes dramatic reprogramming during early embryo development and the establishment of H3K9me3 on LTRs is essential for proper embryo development. Overall design: We mapped the H3K9me3 modifications on embryos from zygote to 8.5 day stage (with separated ICM and TE, Epi and Exe). The mouse metaphase II (MII) oocytes, sperm, as well as mouse embryonic stem cells (mESCs) and mouse trophoblast stem cells (mTSCs) were also analyzed. In the ChIP-seq analysis on pre-implantation embryos, 500 cells were used for per reaction and two or three replicates were performed for each stage. This series contains the Whole Genome Bisulfite-seq data on embryos from zygote to 7.5 day stage (with separated ICM and TE, Epi and Exe).