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H3K27me3-H3K4me1 transition at bivalent promoters instructs lineage specification in development.

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

ORGANISM(S): Mus musculus

PROVIDER: GSE217249 | GEO | 2023/04/05

REPOSITORIES: GEO

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H3K27me3-H3K4me1 transition at bivalent promoters instructs lineage specification in development.

Project description:BackgroundBivalent genes, of which promoters are marked by both H3K4me3 (trimethylation of histone H3 on lysine 4) and H3K27me3 (trimethylation of histone H3 on lysine 27), play critical roles in development and tumorigenesis. Monomethylation on lysine 4 of histone H3 (H3K4me1) is commonly associated with enhancers, but H3K4me1 is also present at promoter regions as an active bimodal or a repressed unimodal pattern. Whether the co-occurrence of H3K4me1 and bivalent marks at promoters plays regulatory role in development is largely unknown.ResultsWe report that in the process of lineage differentiation, bivalent promoters undergo H3K27me3-H3K4me1 transition, the loss of H3K27me3 accompanies by bimodal pattern loss or unimodal pattern enrichment of H3K4me1. More importantly, this transition regulates tissue-specific gene expression to orchestrate the development. Furthermore, knockout of Eed (Embryonic Ectoderm Development) or Suz12 (Suppressor of Zeste 12) in mESCs (mouse embryonic stem cells), the core components of Polycomb repressive complex 2 (PRC2) which catalyzes H3K27 trimethylation, generates an artificial H3K27me3-H3K4me1 transition at partial bivalent promoters, which leads to up-regulation of meso-endoderm related genes and down-regulation of ectoderm related genes, thus could explain the observed neural ectoderm differentiation failure upon retinoic acid (RA) induction. Finally, we find that lysine-specific demethylase 1 (LSD1) interacts with PRC2 and contributes to the H3K27me3-H3K4me1 transition in mESCs.ConclusionsThese findings suggest that H3K27me3-H3K4me1 transition plays a key role in lineage differentiation by regulating the expression of tissue specific genes, and H3K4me1 pattern in bivalent promoters could be modulated by LSD1 via interacting with PRC2.

| S-EPMC10061859 | biostudies-literature

H3K27me3-H3K4me1 transition at bivalent promoters instructs lineage specification in development [RNA-seq]

Project description:To investigate the differential expression pattern between wild type mESC cells and PRC2-deficient cells. We established Eed-KO and Suz12-KO cell lines. We then performed gene expression profiling analysis using data obtained from RNA-seq of these different cells.

2023-04-05 | GSE217248 | GEO

H3K27me3-H3K4me1 transition at bivalent promoters instructs lineage specification in development [ChIP-seq]

Project description:Chromatin immunoprecipitation DNA-sequencing (ChIP-seq) for LSD1 as well as histone modifications H3K4me1, H3K4me3 and H3K27me3 in WT OG2 mESC cells and its KO derivatives (Eed-KO and Suz12-KO ).

2023-04-05 | GSE217247 | GEO

H3K27me3-H3K4me1 transition at bivalent promoters instructs lineage specification in development.

Project description:H3K27me3-H3K4me1 transition at bivalent promoters instructs lineage specification in development.

| PRJNA898276 | ENA

H3K27me3-H3K4me1 transition at bivalent promoters instructs lineage specification in development [RNA-seq]

Project description:H3K27me3-H3K4me1 transition at bivalent promoters instructs lineage specification in development [RNA-seq]

| PRJNA898283 | ENA

H3K27me3-H3K4me1 transition at bivalent promoters instructs lineage specification in development [ChIP-seq]

Project description:H3K27me3-H3K4me1 transition at bivalent promoters instructs lineage specification in development [ChIP-seq]

| PRJNA898281 | ENA

Chromatin landscape instructs precise transcription factor regulome during embryonic lineage specification

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

2024-04-01 | GSE250178 | GEO

Pan-cancer analysis revealed H3K4me1 at bivalent promoters premarks DNA hypermethylation during tumor development and identified the regulatory role of DNA methylation in relation to histone modifications.

Project description:BackgroundDNA hypermethylation at promoter CpG islands (CGIs) is a hallmark of cancers and could lead to dysregulation of gene expression in the development of cancers, however, its dynamics and regulatory mechanisms remain elusive. Bivalent genes, that direct development and differentiation of stem cells, are found to be frequent targets of hypermethylation in cancers.ResultsHere we performed comprehensive analysis across multiple cancer types and identified that the decrease in H3K4me1 levels coincides with DNA hypermethylation at the bivalent promoter CGIs during tumorigenesis. Removal of DNA hypermethylation leads to increment of H3K4me1 at promoter CGIs with preference for bivalent genes. Nevertheless, the alteration of H3K4me1 by overexpressing or knockout LSD1, the demethylase of H3K4, doesn't change the level or pattern of DNA methylation. Moreover, LSD1 was found to regulate the expression of a bivalent gene OVOL2 to promote tumorigenesis. Knockdown of OVOL2 in LSD1 knockout HCT116 cells restored the cancer cell phenotype.ConclusionIn summary, our work identified a universal indicator that can pre-mark DNA hypermethylation in cancer cells, and dissected the interplay between H3K4me1 and DNA hypermethylation in detail. Current study also reveals a novel mechanism underlying the oncogenic role of LSD1, providing clues for cancer therapies.

| S-EPMC10157937 | biostudies-literature

H3K4me1 Distribution Predicts Transcription State and Poising at Promoters.

Project description:Monomethylation on lysine 4 of histone H3 (H3K4me1) is commonly associated with distal enhancers, but H3K4me1 is also present at promoter regions proximal to transcription start sites. To assess a possible role for H3K4me1 in dictating gene regulatory states at promoters, we examined H3K4me1 peak density around promoters in human and mouse germ cells using an analytic strategy that allowed us to assess relationships between different epigenetic marks on a promoter-by-promoter basis. We found that H3K4me1 exhibits either a bimodal pattern at active promoters, where it flanks H3K4me3, or a unimodal pattern at poised promoters, where it coincides with both H3K4me3 and H3K27me3. This pattern is correlated with gene expression level, but is more strongly linked to a poised chromatin state, defined by the simultaneous presence of H3K4me3 and H3K27me3, than to transcriptional activity. The pattern is especially prominent in germ cells, but is also present in other cell types, including embryonic stem cells and differentiated somatic cells. We propose that H3K4me1 is a key feature of the poised epigenetic state, and suggest possible roles for this mark in epigenetic memory.

| S-EPMC7214686 | biostudies-literature

Glutamine metabolism regulates endothelial to hematopoietic transition and hematopoietic lineage specification.

Project description:During hematopoietic development, definitive hematopoietic cells are derived from hemogenic endothelial (HE) cells through a process known as endothelial to hematopoietic transition (EHT). During EHT, transitioning cells proliferate and undergo progressive changes in gene expression culminating in the new cell identity with corresponding changes in function, phenotype and morphology. However, the metabolic pathways fueling this transition remain unclear. We show here that glutamine is a crucial regulator of EHT and a rate limiting metabolite in the hematopoietic differentiation of HE cells. Intriguingly, different hematopoietic lineages require distinct derivatives of glutamine. While both derivatives, α-ketoglutarate and nucleotides, are required for early erythroid differentiation of HE during glutamine deprivation, lymphoid differentiation relies on α-ketoglutarate alone. Furthermore, treatment of HE cells with α-ketoglutarate in glutamine-free conditions pushes their differentiation towards lymphoid lineages both in vitro and in vivo, following transplantation into NSG mice. Thus, we report an essential role for glutamine metabolism during EHT, regulating both the emergence and the specification of hematopoietic cells through its various derivatives.

| S-EPMC8413451 | biostudies-literature

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