ArticleMolecular cell2017
The DNA Damage Checkpoint Eliminates Mouse Oocytes with Chromosome Synapsis Failure.
Article in Molecular cell, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 83 papers.
What it found
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Who cites it
83 citing papers in PubMed, 130 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
- A mammalian-specific domain of MSH5 drives the transition from crossover licensing to designation during meiotic prophase I.bioRxiv : the preprint server for biology · 2026Article
- Structure and function of the synaptonemal complex.The Journal of cell biology · 2026Review
- NFYA regulates two sequential genome-wide transcriptional activation events during oocyte to embryo transition.bioRxiv : the preprint server for biology · 2026Article
- Coordinating meiotic prophase I progression and early oocyte differentiation.Development (Cambridge, England) · 2026Article
- Building a resilient ovarian reserve: Early soma-oocyte interactions.Current topics in developmental biology · 2026Review
- Meiotic Recombination in Teleosts.Advances in experimental medicine and biology · 2026Review
- Evaluating Selective Quality Control in Mammalian Oogenesis: Evidence and Opportunities.Annual review of genetics · 2025Review
- Article
- TRIP13 fosters both transcriptional silencing and DSB repair during meiosis.bioRxiv : the preprint server for biology · 2025Article
- Distinct cellular and reproductive consequences of meiotic chromosome synapsis defects in syce2 and sycp1 mutant zebrafish.PLoS genetics · 2025Article
- CNTD1 is crucial for crossover formation in female meiosis and for establishing the ovarian reserve.The Journal of cell biology · 2025Article
- Single-Cell Transcriptomic Analysis of the Potential Mechanisms of Follicular Development inInternational journal of molecular sciences · 2025Article
- Aberrant activation of chromosome asynapsis checkpoint triggers oocyte elimination.Nature communications · 2025Article
- A simple immunohistochemical method for perinatal mammalian ovaries revealed different kinetics of oocyte apoptosis caused by DNA damage and asynapsis.Histochemistry and cell biology · 2025Article
- Single-cell and bulk transcriptional profiling of mouse ovaries reveals novel genes and pathways associated with DNA damage response in oocytes.Developmental biology · 2025Article
- Defects in meiosis I contribute to the genesis of androgenetic hydatidiform moles.The Journal of clinical investigation · 2024Article
- TRIP13 localizes to synapsed chromosomes and functions as a dosage-sensitive regulator of meiosis.eLife · 2024Article
- Sustained fertility from first-wave follicle oocytes that pause their growth.bioRxiv : the preprint server for biology · 2024Article
23 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
Abstract
Pairing and synapsis of homologous chromosomes during meiosis is crucial for producing genetically normal gametes and is dependent upon repair of SPO11-induced double-strand breaks (DSBs) by homologous recombination. To prevent transmission of genetic defects, diverse organisms have evolved mechanisms to eliminate meiocytes containing unrepaired DSBs or unsynapsed chromosomes. Here we show that the CHK2 (CHEK2)-dependent DNA damage checkpoint culls not only recombination-defective mouse oocytes but also SPO11-deficient oocytes that are severely defective in homolog synapsis. The checkpoint is triggered in oocytes that accumulate a threshold level of spontaneous DSBs (∼10) in late prophase I, the repair of which is inhibited by the presence of HORMAD1/2 on unsynapsed chromosome axes. Furthermore, Hormad2 deletion rescued the fertility of oocytes containing a synapsis-proficient, DSB repair-defective mutation in a gene (Trip13) required for removal of HORMADs from synapsed chromosomes, suggesting that many meiotic DSBs are normally repaired by intersister recombination in mice.
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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.