ArticlePLoS genetics2020
The DNA damage response is required for oocyte cyst breakdown and follicle formation in mice.
Article in PLoS genetics, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 40 citations in OpenAlex.
- Loss of Nemp1 disrupts female meiosis and activates a conserved ATM-CHK2 checkpoint.Nature communications · 2026Article
- Later age of natural menopause among women with the pathogenicJournal of medical genetics · 2026Article
- Cross-species single-cell transcriptomic analyses reveal evolutionary conservation and diversification of ovarian tissues.Journal of animal science and biotechnology · 2026Article
- Acrylamide disrupts meiotic G2/M transition and SAC activity during oocyte maturation.Biology direct · 2026Article
- Maternal sleep deprivation during pregnancy induced offspring germ cells loss through ferroptosis.Cell death discovery · 2025Article
- Evaluating Selective Quality Control in Mammalian Oogenesis: Evidence and Opportunities.Annual review of genetics · 2025Review
- TRIP13 fosters both transcriptional silencing and DSB repair during meiosis.bioRxiv : the preprint server for biology · 2025Article
- Article
- CNTD1 is crucial for crossover formation in female meiosis and for establishing the ovarian reserve.The Journal of cell biology · 2025Article
- Rare SNP in theNAR molecular medicine · 2025Article
- Chromatin remodeler CHD4 establishes chromatin states required for ovarian reserve formation, maintenance and male germ cell survival.Nucleic acids research · 2025Article
- Exocyst complex component 1 (Exoc1) loss in dormant oocyte disrupts c-KIT and growth differentiation factor (GDF9) subcellular localization and causes female infertility in mice.Cell death discovery · 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
- Chromatin remodeler CHD4 establishes chromatin states required for ovarian reserve formation, maintenance, and germ cell survival.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
- Single-cell and bulk transcriptional profiling of mouse ovaries reveals novel genes and pathways associated with DNA damage response in oocytes.bioRxiv : the preprint server for biology · 2024Article
- Steroidogenic factor 1 (SF-1;Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Checkpoint Kinase 1 Is a Key Signal Transducer of DNA Damage in the Early Mammalian Cleavage Embryo.International journal of molecular sciences · 2023Review
- 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
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mammalian oogonia proliferate without completing cytokinesis, forming cysts. Within these, oocytes differentiate and initiate meiosis, promoting double-strand break (DSBs) formation, which are repaired by homologous recombination (HR) causing the pairing and synapsis of the homologs. Errors in these processes activate checkpoint mechanisms, leading to apoptosis. At the end of prophase I, in contrast with what is observed in spermatocytes, oocytes accumulate unrepaired DSBs. Simultaneously to the cyst breakdown, there is a massive oocyte death, which has been proposed to be necessary to enable the individualization of the oocytes to form follicles. Based upon all the above-mentioned information, we hypothesize that the apparently inefficient HR occurring in the oocytes may be a requirement to first eliminate most of the oocytes and enable cyst breakdown and follicle formation. To test this idea, we compared perinatal ovaries from control and mutant mice for the effector kinase of the DNA Damage Response (DDR), CHK2. We found that CHK2 is required to eliminate ~50% of the fetal oocyte population. Nevertheless, the number of oocytes and follicles found in Chk2-mutant ovaries three days after birth was equivalent to that of the controls. These data revealed the existence of another mechanism capable of eliminating oocytes. In vitro inhibition of CHK1 rescued the oocyte number in Chk2-/- mice, implying that CHK1 regulates postnatal oocyte death. Moreover, we found that CHK1 and CHK2 functions are required for the timely breakdown of the cyst and to form follicles. Thus, we uncovered a novel CHK1 function in regulating the oocyte population in mice. Based upon these data, we propose that the CHK1- and CHK2-dependent DDR controls the number of oocytes and is required to properly break down oocyte cysts and form follicles in mammals.
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