ArticleProceedings of the National Academy of Sciences of the United States of America2005
Distinct DNA-damage-dependent and -independent responses drive the loss of oocytes in recombination-defective mouse mutants.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 143 papers.
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Who cites it
143 citing papers in PubMed, 244 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
- Insights into Ovarian Cancer: Unraveling the Role of DNA Double-strand Break-related Genes in Pathogenesis and Therapeutic Avenues.Reproductive sciences (Thousand Oaks, Calif.) · 2026Review
- Coordinating meiotic prophase I progression and early oocyte differentiation.Development (Cambridge, England) · 2026Article
- Meiotic Recombination in Teleosts.Advances in experimental medicine and biology · 2026Review
- Forceful Beginnings: Mechanotransduction and Mechanosensation at the Meiotic Cell Nucleus During Gamete Development.Results and problems in cell differentiation · 2026Review
- Adolescent psychological stress impairs spermatogenesis by disrupting meiotic progression in male mice.PeerJ · 2026Article
- Evaluating Selective Quality Control in Mammalian Oogenesis: Evidence and Opportunities.Annual review of genetics · 2025Review
- Distinct cellular and reproductive consequences of meiotic chromosome synapsis defects in syce2 and sycp1 mutant zebrafish.PLoS genetics · 2025Article
- Mechanisms underlying low mutation rates in mammalian oocytes and preimplantation embryos.Nucleic acids research · 2025Review
- CNTD1 is crucial for crossover formation in female meiosis and for establishing the ovarian reserve.The Journal of cell biology · 2025Article
- Aberrant activation of chromosome asynapsis checkpoint triggers oocyte elimination.Nature communications · 2025Article
- Azoospermia/Oligozoospermia and Prostate Cancer Are Increased in Families of Women With Primary Ovarian Insufficiency.Journal of the Endocrine Society · 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
- An overview of different methods to establish a murine premature ovarian failure model.Animal models and experimental medicine · 2024Review
- Defects in meiosis I contribute to the genesis of androgenetic hydatidiform moles.The Journal of clinical investigation · 2024Article
- Secretome from estrogen-responding human placenta-derived mesenchymal stem cells rescues ovarian function and circadian rhythm in mice with cyclophosphamide-induced primary ovarian insufficiency.Journal of biomedical science · 2024Article
- Sustained fertility from first-wave follicle oocytes that pause their growth.bioRxiv : the preprint server for biology · 2024Article
- Formation and resolution of meiotic chromosome entanglements and interlocks.Journal of cell science · 2024Review
- 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
83 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
Defects in meiotic recombination in many organisms result in arrest because of activation of a meiotic checkpoint(s). The proximal defect that triggers this checkpoint in mammalian germ cells is not understood, but it has been suggested to involve either the presence of DNA damage in the form of unrepaired recombination intermediates or defects in homologous chromosome pairing and synapsis independent of DNA damage per se. To distinguish between these possibilities in the female germ line, we compared mouse oocyte development in a mutant that fails to form the double-strand breaks (DSBs) that initiate meiotic recombination (Spo11-/-) to mutants with defects in processing DSBs when they are formed (Dmc1-/- and Msh5-/-), and we examined the epistasis relationships between these mutations. Absence of DSB formation caused a partial defect in follicle formation, whereas defects in DSB repair caused earlier and more severe meiotic arrest, which could be suppressed by eliminating DSB formation. Therefore, our analysis reveals that there are both DNA-damage-dependent and -independent responses to recombination errors in mammalian oocytes. By using these findings as a paradigm, we also examined oocyte loss in mutants lacking the DNA-damage checkpoint kinase ATM. The absence of ATM caused defects in folliculogenesis that were similar to those in Dmc1 mutants and that could be suppressed by Spo11 mutation, implying that oocyte death in Atm-deficient animals is a response to defective DSB repair.
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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.