Ontology highlight
ABSTRACT:
OTHER RELATED OMICS DATASETS IN: GSE69978
PROVIDER: PRJNA287319 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR2067630.fastq.gz | Fastqsanger.gz | |||
| SRR2067631.fastq.gz | Fastqsanger.gz | |||
| SRR2067632.fastq.gz | Fastqsanger.gz | |||
| SRR2067633.fastq.gz | Fastqsanger.gz | |||
| SRR2067624.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 12 |
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Project description:The major function of Polycomb group proteins (PcG) is to maintain transcriptional repression to preserve cellular identity. This is exerted by two distinct repressive complexes, PRC1 and PRC2, that modify histones by depositing H2AK119ub1 and H3K27me3, respectively. Both complexes are essential for development and are deregulated in several types of human tumors. PRC1 and PRC2 exist in different variants and show a complex regulatory cross-talk. However, the contribution that H2AK119ub1 plays in mediating PcG repressive functions remains largely controversial. Coupling an inducible system with the expression of a fully catalytic inactive RING1B mutant, we demonstrated that H2AK119ub1 deposition is essential to maintain PcG-target genes repressed in ESC. Loss of H2AK119ub1 induced a rapid displacement of PRC2 activity and a loss of H3K27me3 deposition. This affected both PRC2.1 and PRC2.2 variants and further correlated with a strong displacement and destabilization of canonical PRC1. Finally, we find that variant PRC1 forms can sense H2AK119ub1 deposition, which contributes to their stabilization specifically at sites where this modification is highly enriched. Overall our data place H2AK119ub1 deposition as central hub that mount PcG repressive machineries to preserve cell transcriptional identit
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Project description:Mouse ES cells expressing catalytically inactive Ring1B display impaired Ring1B and H3K27me3 deposition.
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Project description:Post-transcriptional regulation mediated by RNA-binding proteins is essential for B cell development and differentiation. EZH2 is a key regulatory protein involved in B cell development and the germinal center response, and its expression is subject to alternative splicing regulation. Skipping of exon 14 in EZH2 disrupts its catalytic activity for H3K27me3 deposition. To identify proteins that regulate EZH2 alternative splicing in B cells, we performed an RNA pull-down assay using exon 14 together with part of intron 14 of EZH2 pre-mRNA, followed by mass spectrometry analysis of the pulled-down proteins.
2026-04-30 | PXD077818 | Pride
Project description:MYCN-amplification is a strong predictor of poor prognosis in neuroblastoma, an embryonal malignancy that accounts for 15% of pediatric cancer deaths. Here, we found that MYCN-amplified neuroblastoma tumors have increased 5-hydroxymethylcytosine (5-hmC) deposition on Polycomb Repressive Complex 2 (PRC2) target genes. 5-hmC and H3K27me3, a catalytic product of PRC2, directly co-localize at the nucleosomal level in MYCN-amplified neuroblastoma. Genes with co-localization of 5-hmC/H3K27me3 are involved in development related pathways and are transcriptionally repressed in MYCN-amplified neuroblastoma. Chemical and genetic inhibition of 5-hmC deposition results in a loss of H3K27me3 deposition on protein-coding genes. Furthermore, 5-hmC deposition predisposes H3K27me3 marked genes to transcriptional activation upon PRC2 inhibition with tazemetostat. Low expression of genes marked by 5-hmC/H3K27me3 is associated with poor clinical outcome. Our results suggest that 5-hmC/H3K27me3 co-operate to repress mediators of development highlighting a novel link between DNA modifications and chromatin modifications with potential therapeutic implications in MYCN-amplified neuroblastoma.
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Project description:MYCN-amplification is a strong predictor of poor prognosis in neuroblastoma, an embryonal malignancy that accounts for 15% of pediatric cancer deaths. Here, we found that MYCN-amplified neuroblastoma tumors have increased 5-hydroxymethylcytosine (5-hmC) deposition on Polycomb Repressive Complex 2 (PRC2) target genes. 5-hmC and H3K27me3, a catalytic product of PRC2, directly co-localize at the nucleosomal level in MYCN-amplified neuroblastoma. Genes with co-localization of 5-hmC/H3K27me3 are involved in development related pathways and are transcriptionally repressed in MYCN-amplified neuroblastoma. Chemical and genetic inhibition of 5-hmC deposition results in a loss of H3K27me3 deposition on protein-coding genes. Furthermore, 5-hmC deposition predisposes H3K27me3 marked genes to transcriptional activation upon PRC2 inhibition with tazemetostat. Low expression of genes marked by 5-hmC/H3K27me3 is associated with poor clinical outcome. Our results suggest that 5-hmC/H3K27me3 co-operate to repress mediators of development highlighting a novel link between DNA modifications and chromatin modifications with potential therapeutic implications in MYCN-amplified neuroblastoma.
2026-05-12 | GSE294307 | GEO
Project description:MYCN-amplification is a strong predictor of poor prognosis in neuroblastoma, an embryonal malignancy that accounts for 15% of pediatric cancer deaths. Here, we found that MYCN-amplified neuroblastoma tumors have increased 5-hydroxymethylcytosine (5-hmC) deposition on Polycomb Repressive Complex 2 (PRC2) target genes. 5-hmC and H3K27me3, a catalytic product of PRC2, directly co-localize at the nucleosomal level in MYCN-amplified neuroblastoma. Genes with co-localization of 5-hmC/H3K27me3 are involved in development related pathways and are transcriptionally repressed in MYCN-amplified neuroblastoma. Chemical and genetic inhibition of 5-hmC deposition results in a loss of H3K27me3 deposition on protein-coding genes. Furthermore, 5-hmC deposition predisposes H3K27me3 marked genes to transcriptional activation upon PRC2 inhibition with tazemetostat. Low expression of genes marked by 5-hmC/H3K27me3 is associated with poor clinical outcome. Our results suggest that 5-hmC/H3K27me3 co-operate to repress mediators of development highlighting a novel link between DNA modifications and chromatin modifications with potential therapeutic implications in MYCN-amplified neuroblastoma.
2026-05-12 | GSE294304 | GEO
Project description:ChIP-seq for H3K27me3 and Ring1B was performed in WT mESCs and mESCs containing catalytically inactive Ring1B (I53A mutant). Cells expressing catalytically inactive Ring1B maintain the spatial distribution of Ring1B and H3K27me3 but at reduced levels. These findings support the notion that PRC2 recruitment is, in part, dependent on H2A ubiquitination (H2AK119ub).
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Project description:ChIP-seq for H3K27me3 and Ring1B was performed in WT mESCs and mESCs containing catalytically inactive Ring1B (I53A mutant). Cells expressing catalytically inactive Ring1B maintain the spatial distribution of Ring1B and H3K27me3 but at reduced levels. These findings support the notion that PRC2 recruitment is, in part, dependent on H2A ubiquitination (H2AK119ub). Two biological replicates were performed for Ring1B and H3K27me3 ChIPs in WT and Ring1B I53A/I53A mouse ESCs. Input chromatin was sequenced for each replicate as a control for ChIP enrichment.
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Project description:Polycomb Repressive Complex 2 (PRC2) deposits H3K27me3 to recruit canonical PRC1 (cPRC1) that establishes repressive heterochromatin. Higher order cPRC1-mediated chromatin interactions characterize early development and resolve during cell differentiation. Here, we use two opposing models of H3K27me3 dysregulation to elucidate how these long-range loops affect gene expression and cellular phenotypes. Aggressive gliomas driven by histone H3 Lys-27-Met (H3K27M) mutations or EZH-Interacting Protein (EZHIP) expression confine H3K27me3 deposition to PRC2 nucleation sites, while loss of the H3K36 methyltransferase NSD1 in pluripotent stem cells leads to its unrestrained spread from these sites. In H3K27M mutant tumours, focal H3K27me3 deposition concentrates chromatin occupancy of cPRC1 complexes, which results in long-range chromatin interactions anchored in polycomb bodies, mirroring patterns found in stem cells. Conversely, spread of H3K27me3 due to NSD1 loss dilutes cPRC1 deposition and disrupts polycomb body architecture. In H3K27M cells, H3K27me3 confinement sustains repression of genes tethered to the polycomb bodies, promoting self-renewing progenitor states required for tumour development. Maintenance of progenitor states depends on cPRC1 interaction with H3K27me3, as chemical allosteric modulation of chromodomains alleviates repression of transcription and promotes differentiation. These results suggest that H3K27me3 spread from CGIs modulates cPRC1 gene expression programs to orchestrate developmental transitions through the maintenance or dissolution of repressive 3D loop architecture at polycomb bodies. Imbalances in the spread of H3K27me3 altering chromatin architecture in disease including H3K27M-expressing neoplasms or following NSD1 loss contribute to explain pathogenic states.
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Project description:Polycomb Repressive Complex 2 (PRC2) deposits H3K27me3 to recruit canonical PRC1 (cPRC1) that establishes repressive heterochromatin. Higher order cPRC1-mediated chromatin interactions characterize early development and resolve during cell differentiation. Here, we use two opposing models of H3K27me3 dysregulation to elucidate how these long-range loops affect gene expression and cellular phenotypes. Aggressive gliomas driven by histone H3 Lys-27-Met (H3K27M) mutations or EZH-Interacting Protein (EZHIP) expression confine H3K27me3 deposition to PRC2 nucleation sites, while loss of the H3K36 methyltransferase NSD1 in pluripotent stem cells leads to its unrestrained spread from these sites. In H3K27M mutant tumours, focal H3K27me3 deposition concentrates chromatin occupancy of cPRC1 complexes, which results in long-range chromatin interactions anchored in polycomb bodies, mirroring patterns found in stem cells. Conversely, spread of H3K27me3 due to NSD1 loss dilutes cPRC1 deposition and disrupts polycomb body architecture. In H3K27M cells, H3K27me3 confinement sustains repression of genes tethered to the polycomb bodies, promoting self-renewing progenitor states required for tumour development. Maintenance of progenitor states depends on cPRC1 interaction with H3K27me3, as chemical allosteric modulation of chromodomains alleviates repression of transcription and promotes differentiation. These results suggest that H3K27me3 spread from CGIs modulates cPRC1 gene expression programs to orchestrate developmental transitions through the maintenance or dissolution of repressive 3D loop architecture at polycomb bodies. Imbalances in the spread of H3K27me3 altering chromatin architecture in disease including H3K27M-expressing neoplasms or following NSD1 loss contribute to explain pathogenic states.
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