ArticlePLoS genetics2016
Maternal Setdb1 Is Required for Meiotic Progression and Preimplantation Development in Mouse.
Article in PLoS genetics, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.
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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.
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Who cites it
57 citing papers in PubMed, 92 citations in OpenAlex.
- The multi-omics regulatory landscape of human early embryogenesis.Cellular and molecular life sciences : CMLS · 2026Review
- The DREAM and MEC NuRD complexes reinforce SPR-5/MET-2 maternal reprogramming to maintain the germline-soma distinction.Genetics · 2026Article
- Article
- Epigenetic remodeling during early embryonic development.Frontiers in cell and developmental biology · 2026Review
- Gonocytes in Transition: Establishing the Male Germline Identity.Advances in experimental medicine and biology · 2026Review
- Ectopic transcription due to inherited histone methylation may interfere with the ongoing function of differentiated neurons.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Article
- UHRF1 in endothelial cells is essential for angiogenesis and associated with the activation of pro-angiogenic signaling pathways and expression of endothelial genes.Angiogenesis · 2025Article
- Epigenetic regulation of iron metabolism and ferroptosis in Parkinson's disease: Identifying novel epigenetic targets.Acta pharmacologica Sinica · 2025Review
- A comprehensive review of histone modifications during mammalian oogenesis and early embryo development.Histochemistry and cell biology · 2025Review
- Essential roles of histone lysine methyltransferases EZH2 and EHMT1 in male embryo development of Phenacoccus solenopsis.Communications biology · 2024Article
- Inheritance of H3K9 methylation regulates genome architecture in Drosophila early embryos.The EMBO journal · 2024Article
- Auto-suppression of Tet dioxygenases protects the mouse oocyte genome from oxidative demethylation.Nature structural & molecular biology · 2024Article
- The function of histone methyltransferase SETDB1 and its roles in liver cancer.Frontiers in cell and developmental biology · 2024Review
- The diverging role of CDC14B: from mitotic exit in yeast to cell fate control in humans.The EMBO journal · 2023Review
- Review
- SPR-1/CoREST facilitates the maternal epigenetic reprogramming of the histone demethylase SPR-5/LSD1.Genetics · 2023Article
- Multi-omics analyses demonstrate a critical role for EHMT1 methyltransferase in transcriptional repression during oogenesis.Genome research · 2023Article
- Expression of the histone lysine methyltransferases SETD1B, SETDB1, SETD2, and CFP1 exhibits significant changes in the oocytes and granulosa cells of aged mouse ovaries.Histochemistry and cell biology · 2022Article
- Epigenetic Reprogramming in Early Animal Development.Cold Spring Harbor perspectives in biology · 2022Review
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 2 countries.
Funding
Abstract
Oocyte meiotic progression and maternal-to-zygote transition are accompanied by dynamic epigenetic changes. The functional significance of these changes and the key epigenetic regulators involved are largely unknown. Here we show that Setdb1, a lysine methyltransferase, controls the global level of histone H3 lysine 9 di-methyl (H3K9me2) mark in growing oocytes. Conditional deletion of Setdb1 in developing oocytes leads to meiotic arrest at the germinal vesicle and meiosis I stages, resulting in substantially fewer mature eggs. Embryos derived from these eggs exhibit severe defects in cell cycle progression, progressive delays in preimplantation development, and degeneration before reaching the blastocyst stage. Rescue experiments by expressing wild-type or inactive Setdb1 in Setdb1-deficient oocytes suggest that the catalytic activity of Setdb1 is essential for meiotic progression and early embryogenesis. Mechanistically, up-regulation of Cdc14b, a dual-specificity phosphatase that inhibits meiotic progression, greatly contributes to the meiotic arrest phenotype. Setdb1 deficiency also leads to derepression of transposons and increased DNA damage in oocytes, which likely also contribute to meiotic defects. Thus, Setdb1 is a maternal-effect gene that controls meiotic progression and is essential for early embryogenesis. Our results uncover an important link between the epigenetic machinery and the major signaling pathway governing meiotic progression.
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Registered trials
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.