ArticleThe Journal of cell biology2025
CNTD1 is crucial for crossover formation in female meiosis and for establishing the ovarian reserve.
Article in The Journal of cell biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Identification of the homozygous truncating mutation inGenes & diseases · 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
- Molecular assessment of recombination processing across genetically diverse mouse strains reveals sexually dimorphic determinants of crossover distribution beyond chromosome length.Molecular biology and evolution · 2026Article
- Ufd2p promotes efficient crossover formation by destabilizing Top2p during meiosis.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Chromosome length is not the sole determinant of sexually dimorphic crossover rates during mammalian meiosis: Insights from genetically diverse mouse strains.bioRxiv : the preprint server for biology · 2025Article
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Authors and funding
7 authors.
Funding
Abstract
In meiotic prophase I, hundreds of DNA double-strand breaks are formed and subsequently repaired as noncrossovers or crossovers (COs). COs are essential for accurate chromosome segregation during the first meiotic division, and errors in this process result in aneuploidy, birth defects, or infertility. Such errors are more pronounced in females compared with males, indicating that CO regulation and surveillance are sexually dimorphic. We demonstrate here dual roles of cyclin N-terminal domain containing 1 (CNTD1) in ensuring appropriate CO between homologous chromosomes in oocytes and in establishing the pool of follicles in the postnatal ovary. CNTD1-deficient oocytes fail to form COs and exhibit a severely depleted follicle pool shortly after birth, which is temporally distinct from previously reported CO mutants. Further investigation indicates that follicle loss is CHK2-dependent, resulting from inappropriate retention of HORMAD1 and the absence of SKP1. These findings indicate that CNTD1 plays novel roles in CO designation and establishment of the follicular reserve in female mammals.
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