Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA325391 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Analysis of changes in gene expression in skin epidermis upon conditional knockout of the essential Polycomb repressive complex 2 (PRC2) subunit Eed. Loss of Eed in skin epithelium leads to de-repression of key Merkel-differentiation genes, which are known PRC2 targets, and results in ectopic formation of Merkel cells that are associated with all hair types. Gene expression analysis: To determine the changes in gene expression in skin epidermis upon conditional knockout of Eed, total RNA was isolated from skin epidermis in four biologic replicates from cells in different conditions and hybridized to SurePrint G3 Mouse GE 8X60K microarrays (Agilent).
2016-06-14 | E-GEOD-83244 | biostudies-arrayexpress
Project description:Analysis of changes in gene expression in skin epidermis upon conditional knockout of the essential Polycomb repressive complex 2 (PRC2) subunit Eed. Loss of Eed in skin epithelium leads to de-repression of key Merkel-differentiation genes, which are known PRC2 targets, and results in ectopic formation of Merkel cells that are associated with all hair types.
2016-06-14 | GSE83244 | GEO
Project description:Aire, a transcriptional regulator whose defect results in the development of autoimmunity, controls the transcriptome in the bulk of medullary thymic epithelial cells (mTECs) including the genes for self-antigens. Mechanisms for this process, however, remained incompletely understood, especially regarding the effects of Aire in each subpopulation in mTECs. Here, we profiled mTECs from EED-cKO (EED conditional knockout mice using Foxn1-Cre, JACKSON LABORATORY #022727 and #018448) and Aire/EED-dKO (Aire EED double knockout mice, PMID: 19015306) by RamDA-seq to evaluate the association between the gene suppression by polycomb repressive complex 2 (PRC2) and the gene induction by Aire. We found that genes are suppressed by PRC2 in an Aire-independent manner in mTEC and the gene suppression by PRC2 paradoxically augments the gene inductions by Aire. Interestingly, PRC2 also suppresses the signature genes for mimetic cell populations and their development was diminished in the absence of EED.
2025-03-12 | GSE249591 | GEO
Project description:Recent studies point to a pivotal role of polycomb repressive complex 2 (PRC2) in stem cell function and cancer. Loss of function approaches targeting individual PRC2 subunits have however generated findings that are difficult to reconcile. Here, we prevent assembly of both Ezh1- and Ezh2-containing PRC2 complexes by conditional deletion of Eed, a core subunit, and assess glodbal gene expression changs in LT-HSCs.
2013-09-24 | GSE51084 | GEO
Project description:The histone methyltransferase Polycomb repressive complex 2 (PRC2) is required for specification of the neural crest, and mis-regulation of neural crest development can cause severe congenital malformations. PRC2 is necessary for neural crest induction, but the embryonic, cellular, and molecular consequences of PRC2 activity after neural crest induction are incompletely understood. Here we show that Eed, a core subunit of PRC2, is required for craniofacial osteoblast differentiation and mesenchymal proliferation after induction of the neural crest. Integrating mouse genetics with single-cell RNA sequencing and epigenomic profiling, our results reveal that conditional knockout of Eed after neural crest cell induction causes severe craniofacial hypoplasia, impaired craniofacial osteogenesis, and attenuated craniofacial mesenchymal cell proliferation that is first evident in post-migratory neural crest cell populations. We show that Eed drives mesenchymal differentiation and proliferation in vivo and in primary craniofacial cell cultures by regulating diverse transcription factor programs that are required for specification of post-migratory neural crest cells. These data enhance understanding of epigenetic mechanisms that underlie craniofacial development, and shed light on the embryonic, cellular, and molecular drivers of rare congenital syndromes in humans.
2025-07-16 | GSE302601 | GEO
Project description:Squamous cell carcinoma (SCC) is a common epithelial malignancy, yet its epigenetic underpinnings remain poorly defined. Here, we identify the Polycomb Repressive Complex 2 (PRC2) as a key epigenetic barrier of SCC tumorigenesis. Despite high EZH2 levels, the PRC2-dependent H3K27me3 is depleted in human and murine SCCs, indicating complex destabilization rather than enzymatic failure. Mechanistically, oncogenic Ras signaling downregulates the PRC2 scaffolding subunit EED, disrupting PRC2 and H3K27me3 and activating oncogenic loci. Depletion of Eed in epidermal progenitors disrupts the proliferation–differentiation balance and, upon carcinogen exposure, drives invasive SCC. Single-cell RNA-seq of Eed-deficient tumors reveals an expansion of tumor-specific keratinocytes and a remodeled pro-tumorigenic microenvironment. Notably, reintroducing EED in SCC cells restores PRC2 integrity and H3K27me3 levels, suppressing tumor growth and mitigating the pro-tumorigenic niche. Our findings establish PRC2 as an essential epigenetic gatekeeper in SCC and suggest restoring PRC2-mediated repression may offer a novel therapeutic strategy.
2026-06-13 | GSE305083 | GEO
Project description:Squamous cell carcinoma (SCC) is a common epithelial malignancy, yet its epigenetic underpinnings remain poorly defined. Here, we identify the Polycomb Repressive Complex 2 (PRC2) as a key epigenetic barrier of SCC tumorigenesis. Despite high EZH2 levels, the PRC2-dependent H3K27me3 is depleted in human and murine SCCs, indicating complex destabilization rather than enzymatic failure. Mechanistically, oncogenic Ras signaling downregulates the PRC2 scaffolding subunit EED, disrupting PRC2 and H3K27me3 and activating oncogenic loci. Depletion of Eed in epidermal progenitors disrupts the proliferation–differentiation balance and, upon carcinogen exposure, drives invasive SCC. Single-cell RNA-seq of Eed-deficient tumors reveals an expansion of tumor-specific keratinocytes and a remodeled pro-tumorigenic microenvironment. Notably, reintroducing EED in SCC cells restores PRC2 integrity and H3K27me3 levels, suppressing tumor growth and mitigating the pro-tumorigenic niche. Our findings establish PRC2 as an essential epigenetic gatekeeper in SCC and suggest restoring PRC2-mediated repression may offer a novel therapeutic strategy.
2026-06-13 | GSE304812 | GEO
Project description:Squamous cell carcinoma (SCC) is a common epithelial malignancy, yet its epigenetic underpinnings remain poorly defined. Here, we identify the Polycomb Repressive Complex 2 (PRC2) as a key epigenetic barrier of SCC tumorigenesis. Despite high EZH2 levels, the PRC2-dependent H3K27me3 is depleted in human and murine SCCs, indicating complex destabilization rather than enzymatic failure. Mechanistically, oncogenic Ras signaling downregulates the PRC2 scaffolding subunit EED, disrupting PRC2 and H3K27me3 and activating oncogenic loci. Depletion of Eed in epidermal progenitors disrupts the proliferation–differentiation balance and, upon carcinogen exposure, drives invasive SCC. Single-cell RNA-seq of Eed-deficient tumors reveals an expansion of tumor-specific keratinocytes and a remodeled pro-tumorigenic microenvironment. Notably, reintroducing EED in SCC cells restores PRC2 integrity and H3K27me3 levels, suppressing tumor growth and mitigating the pro-tumorigenic niche. Our findings establish PRC2 as an essential epigenetic gatekeeper in SCC and suggest restoring PRC2-mediated repression may offer a novel therapeutic strategy.
2026-06-13 | GSE305085 | GEO
Project description:Squamous cell carcinoma (SCC) is a common epithelial malignancy, yet its epigenetic underpinnings remain poorly defined. Here, we identify the Polycomb Repressive Complex 2 (PRC2) as a key epigenetic barrier of SCC tumorigenesis. Despite high EZH2 levels, the PRC2-dependent H3K27me3 is depleted in human and murine SCCs, indicating complex destabilization rather than enzymatic failure. Mechanistically, oncogenic Ras signaling downregulates the PRC2 scaffolding subunit EED, disrupting PRC2 and H3K27me3 and activating oncogenic loci. Depletion of Eed in epidermal progenitors disrupts the proliferation–differentiation balance and, upon carcinogen exposure, drives invasive SCC. Single-cell RNA-seq of Eed-deficient tumors reveals an expansion of tumor-specific keratinocytes and a remodeled pro-tumorigenic microenvironment. Notably, reintroducing EED in SCC cells restores PRC2 integrity and H3K27me3 levels, suppressing tumor growth and mitigating the pro-tumorigenic niche. Our findings establish PRC2 as an essential epigenetic gatekeeper in SCC and suggest restoring PRC2-mediated repression may offer a novel therapeutic strategy.
2026-06-13 | GSE305084 | GEO