ArticleScientific reports2016
Maintenance of the functional integrity of mouse hematopoiesis by EED and promotion of leukemogenesis by EED haploinsufficiency.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 15 citations in OpenAlex.
- Hepatocyte Embryonic Ectoderm Development (Eed) Deficiency Causes Liver Injury, Fibrosis, and Impacts Liver Regeneration.bioRxiv : the preprint server for biology · 2026Article
- Targeting chromatin modifying complexes in acute myeloid leukemia.Stem cells translational medicine · 2025Review
- PTIP epigenetically regulates DNA damage-induced cell cycle arrest by upregulating PRDM1.Scientific reports · 2024Article
- Eed-dependent histone modification orchestrates the iNKT cell developmental program alleviating liver injury.Frontiers in immunology · 2024Article
- Review
- Molecular regulation of hematopoietic stem cell quiescence.Cellular and molecular life sciences : CMLS · 2022Review
- Advances in molecular characterization of myeloid proliferations associated with Down syndrome.Frontiers in genetics · 2022Review
- Review
- Polycomb-like 2 regulates PRC2 components to affect proliferation in glioma cells.Journal of neuro-oncology · 2020Article
- Roles and regulation of histone methylation in animal development.Nature reviews. Molecular cell biology · 2019Review
- PRC2 is high maintenance.Genes & development · 2019Review
- Expression of mutant Asxl1 perturbs hematopoiesis and promotes susceptibility to leukemic transformation.The Journal of experimental medicine · 2018Article
Corrections and comments
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Authors and funding
18 authors at 6 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Polycomb repressive complex 2 (PRC2) participates in transcriptional repression through methylation of histone H3K27. The WD-repeat protein embryonic ectoderm development (EED) is a non-catalytic but an essential component of PRC2 and its mutations were identified in hematopoietic malignancies. To clarify the role(s) of EED in adult hematopoiesis and leukemogenesis, we generated Eed conditional knockout (Eed(Δ/Δ)) mice. Eed(Δ/Δ) mice died in a short period with rapid decrease of hematopoietic cells. Hematopoietic stem/progenitor cells (HSPCs) were markedly decreased with impaired bone marrow (BM) repopulation ability. Cell cycle analysis of HSPCs demonstrated increased S-phase fraction coupled with suppressed G0/G1 entry. Genes encoding cell adhesion molecules are significantly enriched in Eed(Δ/Δ) HSPCs, and consistently, Eed(Δ/Δ) HSPCs exhibited increased attachment to a major extracellular matrix component, fibronectin. Thus, EED deficiency increases proliferation on one side but promotes quiescence possibly by enhanced adhesion to the hematopoietic niche on the other, and these conflicting events would lead to abnormal differentiation and functional defect of Eed(Δ/Δ) HSPCs. In addition, Eed haploinsufficiency induced hematopoietic dysplasia, and Eed heterozygous mice were susceptible to malignant transformation and developed leukemia in cooperation with Evi1 overexpression. Our results demonstrated differentiation stage-specific and dose-dependent roles of EED in normal hematopoiesis and leukemogenesis.
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