ArticleeLife2024
Fetal growth delay caused by loss of non-canonical imprinting is resolved late in pregnancy and culminates in offspring overgrowth.
Article in eLife, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
8 citing papers in PubMed.
- Decoding stage-specific functions of PRC2 in early embryogenesis uncovers roles in preimplantation development and primordial germ cell fate.Nature cell biology · 2026Article
- Metabolic imprinting in trophoblast barrier dysfunction: the role of glucolipotoxicity, endoplasmic reticulum stress, and amino acid transport imbalance.Journal of assisted reproduction and genetics · 2026Review
- Polycomb repressive-deubiquitinase complex safeguards oocyte epigenome and female fertility by restraining Polycomb activity.Nature communications · 2026Article
- Overexpression of placenta-specific noncanonical imprinted genes causes placental enlargement in intersubspecific hybrid mice†.Biology of reproduction · 2026Article
- Decoding the cell intrinsic and extrinsic roles of PRC2 in early embryogenesis.bioRxiv : the preprint server for biology · 2026Article
- Coordinated regulation of chromatin modifiers reflects organised epigenetic programming in mouse oocytes.Epigenetics & chromatin · 2025Article
- Origin, fate and function of extraembryonic tissues during mammalian development.Nature reviews. Molecular cell biology · 2025Review
- Article
Corrections and comments
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Authors and funding
16 authors.
Funding
Abstract
Germline epigenetic programming, including genomic imprinting, substantially influences offspring development. Polycomb Repressive Complex 2 (PRC2) plays an important role in Histone 3 Lysine 27 trimethylation (H3K27me3)-dependent imprinting, loss of which leads to growth and developmental changes in mouse offspring. In this study, we show that offspring from mouse oocytes lacking the PRC2 protein Embryonic Ectoderm Development (EED) were initially developmentally delayed, characterised by low blastocyst cell counts and substantial growth delay in mid-gestation embryos. This initial developmental delay was resolved as offspring underwent accelerated fetal development and growth in late gestation resulting in offspring that were similar stage and weight to controls at birth. The accelerated development and growth in offspring from
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Registered trials
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