Allelic reprogramming of the histone modification H3K4me3 in early mammalian development
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ABSTRACT:
PROVIDER: PRJNA292073 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR2147250.fastq.gz | Fastqsanger.gz | |||
| SRR2147260_1.fastq.gz | Fastqsanger.gz | |||
| SRR2147260_2.fastq.gz | Fastqsanger.gz | |||
| SRR2147241_1.fastq.gz | Fastqsanger.gz | |||
| SRR2147241_2.fastq.gz | Fastqsanger.gz |
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Project description:Histone modifications are considered as fundamental epigenetic regulators that control many crucial cellular processes 1. However, whether these marks can be passed on from gametes to the next generation in mammals is a long-standing question that remains unclear. By developing a highly sensitive approach, STAR ChIP-seq, we provided a panoramic view of the landscape of H3K4me3, a histone hallmark for transcription initiation 2, from developing gametes to postimplantation embryos. Interestingly, we found that upon fertilization, extensive reprogramming occurred on the paternal genome, as few H3K4me3 peaks were observed in zygotes before they reappeared after major zygotic genome activation at the late 2-cell stage. On the maternal genome, we unexpectedly found a non-canonical form of H3K4me3 (ncH3K4me3) in full-grown and mature oocytes, which exists as broad peaks at promoters and a large number of distal loci. Such broad H3K4me3 peaks are in striking contrast to typical sharp H3K4me3 peaks restricted in CpG rich regions of promoters. Interestingly, ncH3K4me3 in oocytes overlaps almost exclusively with partially methylated DNA domains (PMDs). It is then inherited in preimplantation embryos before being erased in the late 2-cell embryos, when canonical H3K4me3 starts to be established. The removal of ncH3K4me3 requires zygotic transcription but is independent of DNA replication mediated passive dilution. Finally, downregulation of H3K4me3 in full-grown oocytes by overexpressing an H3K4me3 demethylase KDM5B is associated with defects in genome silencing. Taken together, these data unveiled inheritance and highly dynamic reprogramming of the epigenome in early mammalian development.
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Project description:Reprogramming of histone modification regulates gene expression and mammal preimplantation development. Trimethylation of lysine 4 on histone 3 (H3K4me3) has unique landscape in mouse oocytes and early embryos. However, the dynamics and function of H3K4me3 in livestock embryos remain unclear. To address how it is reprogrammed in domestic animals, we profiled changes of H3K4me3 during bovine early embryo development. Notably, the overall signal of H3K4me3 decreased during embryonic genome activation (EGA). By utilizing ultra-low-input native ChIP-seq (ULI-NChIP-seq) technology, we observed widespread broad H3K4me3 domains in oocytes and embryos. The signal of broad H3K4me3 began to decrease after fertilization and was lowest after EGA. Along with the removal of broad H3K4me3, deposition of H3K4me3 at promoter regions enhanced gradually. Besides, the transcriptional activity and signal of promoter H3K4me3 showed positive correlation after the erasure of broad H3K4me3 at 16-cell stage. Moreover, knocking down of demethylases KDM5A, KDM5B and KDM5C caused EGA delay and blastocyst formation failure. RNA-seq analysis revealed 47.8% down-regulated genes in knockdown embryos at 8/16-cell stage were EGA genes, and 63.1% of up-regulated genes were maternal transcripts. Particularly, the positive correlation between transcriptional activity and promoter H3K4me3 during EGA was restrained when knocking down of KDM5A, KDM5B and KDM5C. Overall, our work initiatively mapped the genomic reprogramming of H3K4me3 during bovine preimplantation development, and KDM5A/B/C played roles in modulating oocyte-to-embryonic transition (OET) through timely erasure of broad H3K4me3 domains far away from promoters.
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