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

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

PROVIDER: PRJNA642903 | ENA |

REPOSITORIES: ENA

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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

| PRJNA642900 | ENA

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)

| PRJNA664996 | ENA

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

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

| PRJNA642902 | ENA

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

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 | GSE158360 | GEO

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

2021-03-15 | GSE153530 | GEO

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

2021-03-15 | GSE153529 | GEO

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: Not available

| S-EPMC8092361 | biostudies-literature

ChIPseq on H3K27ac, H3K27me3 and H2AK119Ub on TXY cell line

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

| PRJNA478785 | ENA

YTHDF1 facilitates PRC1 mediated H2AK119ub in Human ES Cells

Project description:Polycomb repressive complexes( PRCs) play critical role in cell fate decisions during normal development as well as disease progression through mediate histone modifications such as H3K27me3 and H2AK119ub. How exactly PRCs recruited to chromatin remains to be fully illuminated. Here, we report that YTHDF1, a N6-methyladenine (m6A) RNA reader previously known being mainly cytoplasmic, associates with RNF2, a PRC1 protein that mediates H2AK119ub in human embryonic stem cells (hESCs). Specifically, a portion of YTHDF1 localizes in the nuclei and associates with RNF2/ H2AK119ub on a subset of gene loci related to neural development functions. Knock-down YTHDF1 attenuates H2AK119ub modification on these genes and promotes neural differentiation in hESCs. Our findings provide another non-canonical mechanism of YTHDF1 to participate in PRC1 mediated chromatin modification in hESCs.

2023-12-30 | GSE204824 | GEO

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