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METTL14 Regulates Chromatin Bivalent Domains in Mouse Embryonic Stem Cells.

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE206735 | GEO | 2023/06/19

REPOSITORIES: GEO

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METTL14 Regulates Chromatin Bivalent Domains in Mouse Embryonic Stem Cells [ChIP-seq]

Project description:METTL14 (methyltransferase-like 14) is an RNA binding protein that partners with METTL3 to mediate N6-methyladenosine (m6A) methylation of mRNA. Recent studies identified a function for METTL3 in heterochromatin and transcription, but the role of METTL14 in these contexts remains unclear. Here we show that METTL14 binds and regulates mouse embryonic stem cell bivalent domains, which are marked with tri-methylation at lysine 27 of histone H3 (H3K27me3) and tri-methylation at lysine 4 of histone H3 (H3K4me3). Knockout of Mettl14 results in decreased H3K27me3 but increased H3K4me3 levels at bivalent regions, resulting in the resolution of the bivalency and in increased transcription. We demonstrate that bivalent domain regulation by METTL14 is independent of METTL3 or m6A modification. Instead, METTL14 enhances H3K27me3 and reduces H3K4me3 by interacting with and probably recruiting the histone 3 lysine 27 (H3K27) methyltransferase complex PRC2 and the histone 3 lysine 4 (H3K4) demethylases KDM5B to chromatin. Our findings identify a METTL3-independent function of METTL14, important for maintaining the bivalent domains in mESCs, thus revealing a new mechanism of bivalent domain regulation in mammals.

2023-06-19 | GSE206730 | GEO

METTL14 Regulates Chromatin Bivalent Domains in Mouse Embryonic Stem Cells [RNA-seq]

2023-06-19 | GSE206734 | GEO

Asf1a resolves bivalent chromatin domains for the induction of lineage-specific genes during mouse embryonic stem cell differentiation.

Project description:Bivalent chromatin domains containing repressive H3K27me3 and active H3K4me3 modifications are barriers for the expression of lineage-specific genes in ES cells and must be resolved for the transcription induction of these genes during differentiation, a process that remains largely unknown. Here, we show that Asf1a, a histone chaperone involved in nucleosome assembly and disassembly, regulates the resolution of bivalent domains and activation of lineage-specific genes during mouse ES cell differentiation. Deletion of Asf1a does not affect the silencing of pluripotent genes, but compromises the expression of lineage-specific genes during ES cell differentiation. Mechanistically, the Asf1a-histone interaction, but not the role of Asf1a in nucleosome assembly, is required for gene transcription. Asf1a is recruited to several bivalent promoters, partially through association with transcription factors, and mediates nucleosome disassembly during differentiation. We suggest that Asf1a-mediated nucleosome disassembly provides a means for resolution of bivalent domain barriers for induction of lineage-specific genes during differentiation.

| S-EPMC6142193 | biostudies-literature

Nono, a novel bivalent domain factor, regulates Erk signaling and mouse embryonic stem cell pluripotency

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

2016-10-18 | GSE86818 | GEO

Nono, a Bivalent Domain Factor, Regulates Erk Signaling and Mouse Embryonic Stem Cell Pluripotency.

Project description:Nono is a component of the para-speckle, which stores and processes RNA. Mouse embryonic stem cells (mESCs) lack para-speckles, leaving the function of Nono in mESCs unclear. Here, we find that Nono functions as a chromatin regulator cooperating with Erk to regulate mESC pluripotency. We report that Nono loss results in robust self-renewing mESCs with epigenomic and transcriptomic features resembling the 2i (GSK and Erk inhibitors)-induced "ground state." Erk interacts with and is required for Nono localization to a subset of bivalent genes that have high levels of poised RNA polymerase. Nono loss compromises Erk activation and RNA polymerase poising at its target bivalent genes in undifferentiated mESCs, thus disrupting target gene activation and differentiation. These findings argue that Nono collaborates with Erk signaling to regulate the integrity of bivalent domains and mESC pluripotency.

| S-EPMC5086807 | biostudies-literature

Uhrf1 regulates active transcriptional marks at bivalent domains in pluripotent stem cells through Setd1a

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

2018-05-02 | GSE113915 | GEO

H3K4/H3K9me3 Bivalent Chromatin Domains Targeted by Lineage-specific DNA Methylation Pauses Adipocyte Differentiation

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2015-11-19 | E-GEOD-73434 | biostudies-arrayexpress

Dzip3 regulates developmental genes in mouse embryonic stem cells by reorganizing 3D chromatin conformation

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2015-12-08 | E-GEOD-71884 | biostudies-arrayexpress

The Mll2 branch of the COMPASS family regulates bivalent promoters in mouse embryonic stem cells.

Project description:Promoters of many developmentally regulated genes, in the embryonic stem cell state, have a bivalent mark of H3K27me3 and H3K4me3, proposed to confer precise temporal activation upon differentiation. Although Polycomb repressive complex 2 is known to implement H3K27 trimethylation, the COMPASS family member responsible for H3K4me3 at bivalently marked promoters was previously unknown. Here, we identify Mll2 (KMT2b) as the enzyme catalyzing H3K4 trimethylation at bivalentlymarked promoters in embryonic stem cells. Although H3K4me3 at bivalent genes is proposed to prime future activation, we detected no substantial defect in rapid transcriptional induction after retinoic acid treatment in Mll2-depleted cells. Our identification of the Mll2 complex as the COMPASS family member responsible for H3K4me3 marking bivalent promoters provides an opportunity to reevaluate and experimentally test models for the function of bivalency in the embryonic stem cell state and in differentiation.

| S-EPMC3805109 | biostudies-literature

Bivalent chromatin marks developmental regulatory genes in the mouse embryonic germline in vivo.

Project description:Developmental regulatory genes have both activating (H3K4me3) and repressive (H3K27me3) histone modifications in embryonic stem cells (ESCs). This bivalent configuration is thought to maintain lineage commitment programs in a poised state. However, establishing physiological relevance has been complicated by the high number of cells required for chromatin immunoprecipitation (ChIP). We developed a low-cell-number chromatin immunoprecipitation (low-cell ChIP) protocol to investigate the chromatin of mouse primordial germ cells (PGCs). Genome-wide analysis of embryonic day 11.5 (E11.5) PGCs revealed H3K4me3/H3K27me3 bivalent domains highly enriched at developmental regulatory genes in a manner remarkably similar to ESCs. Developmental regulators remain bivalent and transcriptionally silent through the initiation of sexual differentiation at E13.5. We also identified >2,500 "orphan" bivalent domains that are distal to known genes and expressed in a tissue-specific manner but silent in PGCs. Our results demonstrate the existence of bivalent domains in the germline and raise the possibility that the somatic program is continuously maintained as bivalent, potentially imparting transgenerational epigenetic inheritance.

| S-EPMC3700580 | biostudies-literature

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