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SETD2 regulates the maternal epigenome, genomic imprinting and embryonic development [Bisulfite-seq]

ABSTRACT: SETD2 regulates the maternal epigenome, genomic imprinting and embryonic development [Bisulfite-seq]

PROVIDER: PRJNA449121 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6956500_1.fastq.gz	Fastqsanger.gz
	SRR6956500_2.fastq.gz	Fastqsanger.gz
	SRR6956501_1.fastq.gz	Fastqsanger.gz
	SRR6956501_2.fastq.gz	Fastqsanger.gz
	SRR6956502_1.fastq.gz	Fastqsanger.gz

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SETD2 regulates the maternal epigenome, genomic imprinting and embryonic development [Bisulfite-seq]

Project description:The oocyte epigenome plays critical roles in mammalian gametogenesis and embryogenesis. Yet, how it is established remains elusive. Here, we report that histone-lysine N-methyltransferase SETD2, an H3K36me3 methyltransferase, is a crucial regulator of the mouse oocyte epigenome. Deficiency in Setd2 leads to extensive alterations of the oocyte epigenome, including the loss of H3K36me3, failure in establishing the correct DNA methylome, invasion of H3K4me3 and H3K27me3 into former H3K36me3 territories and aberrant acquisition of H3K4me3 at imprinting control regions instead of DNA methylation. Importantly, maternal depletion of SETD2 results in oocyte maturation defects and subsequent one-cell arrest after fertilization. The preimplantation arrest is mainly due to a maternal cytosolic defect, since it can be largely rescued by normal oocyte cytosol. However, chromatin defects, including aberrant imprinting, persist in these embryos, leading to embryonic lethality after implantation. Thus, these data identify SETD2 as a crucial player in establishing the maternal epigenome that in turn controls embryonic development.

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SETD2 regulates the maternal epigenome, genomic imprinting and embryonic development [ChIP-seq]

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Genomic imprinting of Xist by maternal H3K27me3

Project description:Maternal imprinting at the Xist gene is essential to achieve paternal allele-specific imprinted X chromosome inactivation (XCI) in female mammals. However, the mechanism underlying the Xist imprinting is unclear. Here we show that the Xist gene is coated with H3K27me3 in mouse oocytes, which persists through preimplantation development. Ectopic removal of H3K27me3 induces maternal Xist expression and maternal XCI, indicating that maternal H3K27me3 is the imprinting mark of Xist.

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