ArticleNucleic acids research2022
Chromosomal synapsis defects can trigger oocyte apoptosis without elevating numbers of persistent DNA breaks above wild-type levels.
Article in Nucleic acids research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 17 citations in OpenAlex.
- NEMP1 organizes the meiotic telomere-LINC interface to control chromosome movement and telomere integrity.bioRxiv : the preprint server for biology · 2026Article
- 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
- Digital Chromosome Banding Reveals Distinct Spatiotemporal Dynamics and Sexual Dimorphism in Meiotic Silencing.bioRxiv : the preprint server for biology · 2026Article
- Coordinating meiotic prophase I progression and early oocyte differentiation.Development (Cambridge, England) · 2026Article
- 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
- FIGNL1-FIRRM is essential for meiotic recombination and prevents DNA damage-independent RAD51 and DMC1 loading.Nature communications · 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
- Seeding the meiotic DNA break machinery and initiating recombination on chromosome axes.Nature communications · 2024Article
- Heat shock factor 5 establishes the male germ-line meiotic sex chromosome inactivation through regulation ofHeliyon · 2023Article
- Genetic control of meiosis surveillance mechanisms in mammals.Frontiers in cell and developmental biology · 2023Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Generation of haploid gametes depends on a modified version of homologous recombination in meiosis. Meiotic recombination is initiated by single-stranded DNA (ssDNA) ends originating from programmed DNA double-stranded breaks (DSBs) that are generated by the topoisomerase-related SPO11 enzyme. Meiotic recombination involves chromosomal synapsis, which enhances recombination-mediated DSB repair, and thus, crucially contributes to genome maintenance in meiocytes. Synapsis defects induce oocyte apoptosis ostensibly due to unrepaired DSBs that persist in asynaptic chromosomes. In mice, SPO11-deficient oocytes feature asynapsis, apoptosis and, surprisingly, numerous foci of the ssDNA-binding recombinase RAD51, indicative of DSBs of unknown origin. Hence, asynapsis is suggested to trigger apoptosis due to inefficient DSB repair even in mutants that lack programmed DSBs. By directly detecting ssDNAs, we discovered that RAD51 is an unreliable marker for DSBs in oocytes. Further, SPO11-deficient oocytes have fewer persistent ssDNAs than wild-type oocytes. These observations suggest that oocyte quality is safeguarded in mammals by a synapsis surveillance mechanism that can operate without persistent ssDNAs.
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