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

ABSTRACT: 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 ).

ORGANISM(S): Mus musculus

PROVIDER: GSE217247 | GEO | 2023/04/05

REPOSITORIES: GEO

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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.

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.

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CUT&RUN of H3K4me1 in mESC

Project description:Profiling of H3K4me1 genome wide occupancy in mESC WT, LSD1 KO, and rescued with WT LSD1 (RO) and with mutant LSD1 (AK) to explore the effects of LSD1 on histone methylation.

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

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

2023-04-05 | GSE217249 | GEO

The Polycomb Group Protein Suz12 Is Required for Embryonic Stem Cell Differentiation

Project description:Polycomb group (PcG) proteins form multiprotein complexes, called Polycomb repressive complexes (PRCs). PRC2 contains the PcG proteins EZH2, SUZ12, and EED and represses transcription through methylation of lysine (K) 27 of histone H3 (H3). Suz12 is essential for PRC2 activity and its inactivation results in early lethality of mouse embryos. Total RNA was extracted independently from three WT and three Suz12 KO ES cell clones. RNA was quantified, and equal amounts fromthe three Suz12 WT and the three Suz12 KO samples were pooled into one sample to reduce the experimental variation. Targets for microarray hybridization were synthesized according to the supplier’s instructions (Affymetrix). Hybridization, washing, staining, scanning, and data analysis were performed at the Affymetrix microarray unit at the Institute of Molecular Oncology of the Italian Foundation for Cancer Research-European Institute of Oncology campus, Milan, Italy, according to the manufacturer’s instructions.

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

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

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Identification of a novel role of MTF2 in the regulation of H3K27me3 by PRC2 (RNA-Seq)

Project description:We sequenced mRNA from F9 cells after knockdown of EZH2, SUZ12 and EED by shRNA. EZH2, SUZ12 and EED are the core componnets of PRC2 which repress its target genes by H3K27me3.

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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:Background: DNA 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. Results: Here 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. Conclusion: In 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.

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