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Distinct dynamics and functions of H2AK119ub and H3K27me3 in mouse preimplantation embryos (CUT&RUN)

ABSTRACT: Distinct dynamics and functions of H2AK119ub and H3K27me3 in mouse preimplantation embryos (CUT&RUN)

PROVIDER: PRJNA642902 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12112800_1.fastq.gz	Fastqsanger.gz
	SRR12112800_2.fastq.gz	Fastqsanger.gz
	SRR12112801_1.fastq.gz	Fastqsanger.gz
	SRR12112801_2.fastq.gz	Fastqsanger.gz
	SRR12112802_1.fastq.gz	Fastqsanger.gz

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Distinct dynamics and functions of H2AK119ub and H3K27me3 in mouse preimplantation embryos (CUT&RUN)

Project description:Polycomb repressive complexes 1 and 2 (PRC1/2) maintain transcriptional silencing of developmental genes largely by catalyzing mono-ubiquitination of histone H2A at lysine 119 (H2AK119ub1) and trimethylation of histone H3 at lysine 27 (H3K27me3), respectively. How Polycomb domains are reprogrammed during mammalian preimplantation development remains largely unclear. Here we show that, although H2AK119ub1 and H3K27me3 are highly colocalized in gametes, they undergo differential reprogramming dynamics following fertilization. H3K27me3 maintains thousands of maternally biased domains up to the blastocyst stage, whereas maternally biased H2AK119ub1 distribution in zygotes is largely equalized at the two-cell stage. Notably, while maternal PRC2 depletion has a limited effect on global H2AK119ub1 in early embryos, it disrupts allelic H2AK119ub1 at H3K27me3 imprinting loci including Xist. By contrast, acute H2AK119ub1 depletion in zygotes does not affect H3K27me3 imprinting maintenance, at least by the four-cell stage. Importantly, loss of H2AK119ub1, but not H3K27me3, causes premature activation of developmental genes during zygotic genome activation (ZGA) and subsequent embryonic arrest. Thus, our study reveals distinct dynamics and functions of H3K27me3 and H2AK119ub1 in mouse preimplantation embryos.

2021-03-15 | GSE153529 | GEO

Distinct dynamics and functions of H2AK119ub and H3K27me3 in mouse preimplantation embryos

Project description:Distinct dynamics and functions of H2AK119ub and H3K27me3 in mouse preimplantation embryos

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Distinct dynamics and functions of H2AK119ub and H3K27me3 in mouse preimplantation embryos (RNA-Seq)

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Distinct dynamics and functions of H2AK119ub and H3K27me3 in mouse preimplantation embryos (STAR-ChIP)

2021-03-15 | GSE158360 | GEO

Distinct dynamics and functions of H2AK119ub and H3K27me3 in mouse preimplantation embryos (STAR-ChIP)

Project description:Distinct dynamics and functions of H2AK119ub and H3K27me3 in mouse preimplantation embryos (STAR-ChIP)

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Distinct dynamics and functions of H2AK119ub and H3K27me3 in mouse preimplantation embryos (RNA-Seq)

Project description:Distinct dynamics and functions of H2AK119ub and H3K27me3 in mouse preimplantation embryos (RNA-Seq)

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Distinct dynamics and functions of H2AK119ub and H3K27me3 in mouse preimplantation embryos

Project description:This SuperSeries is composed of the SubSeries listed below.

2021-03-15 | GSE153531 | GEO

Distinct dynamics and functions of H2AK119ub1 and H3K27me3 in mouse preimplantation embryos.

Project description:Polycomb repressive complexes 1 and 2 (PRC1/2) maintain transcriptional silencing of developmental genes largely by catalyzing the formation of mono-ubiquitinated histone H2A at lysine 119 (H2AK119ub1) and trimethylated histone H3 at lysine 27 (H3K27me3), respectively. How Polycomb domains are reprogrammed during mammalian preimplantation development remains largely unclear. Here we show that, although H2AK119ub1 and H3K27me3 are highly colocalized in gametes, they undergo differential reprogramming dynamics following fertilization. H3K27me3 maintains thousands of maternally biased domains until the blastocyst stage, whereas maternally biased H2AK119ub1 distribution in zygotes is largely equalized at the two-cell stage. Notably, while maternal PRC2 depletion has a limited effect on global H2AK119ub1 in early embryos, it disrupts allelic H2AK119ub1 at H3K27me3 imprinting loci including Xist. By contrast, acute H2AK119ub1 depletion in zygotes does not affect H3K27me3 imprinting maintenance, at least by the four-cell stage. Importantly, loss of H2AK119ub1, but not H3K27me3, causes premature activation of developmental genes during zygotic genome activation (ZGA) and subsequent embryonic arrest. Thus, our study reveals distinct dynamics and functions of H3K27me3 and H2AK119ub1 in mouse preimplantation embryos.

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Maternal Smchd1 regulates Hox gene expression and patterning in the mouse embryo [H2AK119ub CUT&RUN]

Project description:Parents transmit genetic and epigenetic information to their offspring. Maternal effect genes regulate the offspring epigenome to ensure normal development. Here we report that the epigenetic regulator SMCHD1 has a maternal effect on Hox gene expression and skeletal patterning. Maternal SMCHD1, present in the oocyte and preimplantation embryo, prevents precocious activation of Hox genes post-implantation. Without maternal SMCHD1, highly penetrant posterior homeotic transformations occur in the embryo. Hox genes are decorated with Polycomb marks H2AK119ub and H3K27me3 from the oocyte throughout early embryonic development; however, loss of maternal SMCHD1 does not deplete these marks. Therefore, we propose maternal SMCHD1 acts downstream of Polycomb marks to establish a chromatin state necessary for persistent epigenetic silencing and appropriate Hox gene expression later in the developing embryo. This is a striking role for maternal SMCHD1 in long-lived epigenetic effects impacting offspring phenotype.

2022-06-27 | GSE183739 | GEO

ChIPseq on H3K27ac, H3K27me3 and H2AK119Ub on TXY cell line

Project description:ChIPseq on H3K27ac, H3K27me3 and H2AK119Ub on TXY cell line

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