ArticleClinical epigenetics2018
Loss of maternal EED results in postnatal overgrowth.
Article in Clinical epigenetics, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 45 citations in OpenAlex.
- Decoding stage-specific functions of PRC2 in early embryogenesis uncovers roles in preimplantation development and primordial germ cell fate.Nature cell biology · 2026Article
- Identification and functional characterization of a SUZ12 frameshift variant in a Chinese family with Imagawa-Matsumoto syndrome.BMC medical genomics · 2026Article
- A review of the association between abnormal body mass index and oocyte quality.Journal of ovarian research · 2026Review
- T-Cell Immunosenescence in Systemic Lupus Erythematosus: Molecular Mechanisms and Therapeutic Perspectives.Clinical reviews in allergy & immunology · 2026Review
- Decoding the cell intrinsic and extrinsic roles of PRC2 in early embryogenesis.bioRxiv : the preprint server for biology · 2026Article
- Review
- Histone H3K36 methyltransferases NSD1 and SETD2 are required for brain development.Human genetics · 2025Article
- Coordinated regulation of chromatin modifiers reflects organised epigenetic programming in mouse oocytes.Epigenetics & chromatin · 2025Article
- Mechanistic insights and biomarker discovery in immune cell aging and age-associated diseases.Frontiers in immunology · 2025Review
- Creation of true interspecies hybrids: Rescue of hybrid class with hybrid cytoplasm affecting growth and metabolism.Science advances · 2024Article
- Article
- BAP1 is required prenatally for differentiation and maintenance of postnatal murine enteric nervous system.The Journal of clinical investigation · 2024Article
- Growth disorders caused by variants in epigenetic regulators: progress and prospects.Frontiers in endocrinology · 2024Review
- Research advances of polycomb group proteins in regulating mammalian development.Frontiers in cell and developmental biology · 2024Review
- Roles of endogenous retroviral elements in the establishment and maintenance of imprinted gene expression.Frontiers in cell and developmental biology · 2024Review
- Review
- Article
- Epigenetic regulation of embryonic ectoderm development in stem cell differentiation and transformation during ontogenesis.Cell proliferation · 2023Review
- Inhibition of EED activity enhances cell survival of female germline stem cell and improves the oocytes production during oogenesisOpen biology · 2023Article
- Transient Polycomb activity represses developmental genes in growing oocytes.Clinical epigenetics · 2022Article
Corrections and comments
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Authors and funding
8 authors at 5 institutions in 3 countries.
Funding
Abstract
backgroundInvestigating how epigenetic information is transmitted through the mammalian germline is the key to understanding how this information impacts on health and disease susceptibility in offspring. EED is essential for regulating the repressive histone modification, histone 3 lysine 27 tri-methylation (H3K27me3) at many developmental genes.
resultsIn this study, we used oocyte-specific Zp3-Cre recombinase (Zp3Cre) to delete Eed specifically in mouse growing oocytes, permitting the study of EED function in oocytes and the impact of depleting EED in oocytes on outcomes in offspring. As EED deletion occurred only in growing oocytes and females were mated to normal wild type males, this model allowed the study of oocyte programming without confounding factors such as altered in utero environment. Loss of EED from growing oocytes resulted in a significant overgrowth phenotype that persisted into adult life. Significantly, this involved increased adiposity (total fat) and bone mineral density in offspring. Similar overgrowth occurs in humans with Cohen-Gibson (OMIM 617561) and Weaver (OMIM 277590) syndromes, that result from de novo germline mutations in EED or its co-factor EZH2, respectively. Consistent with a role for EZH2 in human oocytes, we demonstrate that de novo germline mutations in EZH2 occurred in the maternal germline in some cases of Weaver syndrome. However, deletion of Ezh2 in mouse oocytes resulted in a distinct phenotype compared to that resulting from oocyte-specific deletion of Eed.
conclusionsThis study provides novel evidence that altering EED-dependent oocyte programming leads to compromised offspring growth and development in the next generation.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.