ArticleNature communications2020
The BCL-2 pathway preserves mammalian genome integrity by eliminating recombination-defective oocytes.
Article in Nature communications, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
What it found
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Who cites it
23 citing papers in PubMed, 46 citations in OpenAlex.
- Loss of Nemp1 disrupts female meiosis and activates a conserved ATM-CHK2 checkpoint.Nature communications · 2026Article
- SYCP2 recruits HORMAD2 to chromosome axes for unsynapsed chromatin silencing and synapsis surveillance in meiosis.Nature communications · 2026Article
- Comparative developmental competence and gene expression in laparoscopically retrieved- and abattoir-derived goat oocytes.Frontiers in veterinary science · 2026Article
- Maternal age and genome-wide failure of meiotic recombination are associated with triploid conceptions in humans.American journal of human genetics · 2025Article
- Initiation of meiosis from human iPSCs under defined conditions through identification of regulatory factors.Science advances · 2025Article
- Aberrant activation of chromosome asynapsis checkpoint triggers oocyte elimination.Nature communications · 2025Article
- Chlorogenic Acid Ameliorates Chronic Unpredictable Stress-Induced Diminished Ovarian Reserve Through Ovarian Renin-Angiotensin System.Molecular nutrition & food research · 2025Article
- Chromatin remodeler CHD4 establishes chromatin states required for ovarian reserve formation, maintenance and male germ cell survival.Nucleic acids research · 2025Article
- Premeiotic deletion of Eif2s2 causes oocyte arrest at the early diplotene stage and apoptosis in mice.Cell proliferation · 2024Article
- The role of declining ataxia-telangiectasia-mutated (ATM) function in oocyte aging.Cell death discovery · 2024Article
- Induction of Meiosis from Human Pluripotent Stem Cells.bioRxiv : the preprint server for biology · 2024Article
- BRCA1 safeguards genome integrity by activating chromosome asynapsis checkpoint to eliminate recombination-defective oocytes.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- A matter of new life and cell death: programmed cell death in the mammalian ovary.Journal of biomedical science · 2024Review
- SRSF1 regulates primordial follicle formation and number determination during meiotic prophase I.BMC biology · 2023Article
- TP63 gain-of-function mutations cause premature ovarian insufficiency by inducing oocyte apoptosis.The Journal of clinical investigation · 2023Article
- Regulation of Oocyte Apoptosis: A View from Gene Knockout Mice.International journal of molecular sciences · 2023Review
- Genetic control of meiosis surveillance mechanisms in mammals.Frontiers in cell and developmental biology · 2023Review
- Chromosomal synapsis defects can trigger oocyte apoptosis without elevating numbers of persistent DNA breaks above wild-type levels.Nucleic acids research · 2022Article
- Genome diversity and instability in human germ cells and preimplantation embryos.Seminars in cell & developmental biology · 2021Article
- Regulation of Meiotic Prophase One in Mammalian Oocytes.Frontiers in cell and developmental biology · 2021Review
Corrections and comments
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Authors and funding
12 authors at 4 institutions in 4 countries.
Funding
Abstract
DNA double-strand breaks (DSBs) are toxic to mammalian cells. However, during meiosis, more than 200 DSBs are generated deliberately, to ensure reciprocal recombination and orderly segregation of homologous chromosomes. If left unrepaired, meiotic DSBs can cause aneuploidy in gametes and compromise viability in offspring. Oocytes in which DSBs persist are therefore eliminated by the DNA-damage checkpoint. Here we show that the DNA-damage checkpoint eliminates oocytes via the pro-apoptotic BCL-2 pathway members Puma, Noxa and Bax. Deletion of these factors prevents oocyte elimination in recombination-repair mutants, even when the abundance of unresolved DSBs is high. Remarkably, surviving oocytes can extrude a polar body and be fertilised, despite chaotic chromosome segregation at the first meiotic division. Our findings raise the possibility that allelic variants of the BCL-2 pathway could influence the risk of embryonic aneuploidy.
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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.