ArticleCell death and differentiation2020
NBS1 is required for SPO11-linked DNA double-strand break repair in male meiosis.
Article in Cell death and differentiation, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 61 citations in OpenAlex.
- MRE11 suppresses germline mutagenesis at meiotic double-strand breaks in mice.Genes & development · 2026Article
- TPTE, a testis-specific PTEN family member, drives spermatogenesis via PI(4,5)PCell death & disease · 2026Article
- MRE11 suppresses germline mutagenesis at meiotic double-strand breaks in mice.bioRxiv : the preprint server for biology · 2026Article
- Mechanism and potential therapeutic strategies of genetic abnormalities involved in deoxyribonucleic acid double-strand breaks leading to the development of human non-obstructive azoospermia.Reproductive biology and endocrinology : RB&E · 2026Review
- Translesion polymerases and DNA-protein crosslink repair shapes the cellular response to formaldehyde-induced DNA damage in ssDNA.Nucleic acids research · 2025Article
- Insight into meiotic DNA end resection: Mechanisms and regulation.DNA repair · 2025Review
- Lactylation-mediated miRNA regulation in cancer therapy resistance.Journal of translational medicine · 2025Review
- DNA damage response and cell fate decisions across the lifespan: from fetal development to age-related respiratory diseases.Cell & bioscience · 2025Review
- SPO11 cuts!Cell research · 2025Article
- An essential role of the E3 ubiquitin ligase RNF126 in ensuring meiosis I completion during spermatogenesis.Journal of advanced research · 2025Article
- Phospho-TRIM21 orchestrates RPA2 ubiquitination switch to promote homologous recombination and tumor radio/chemo-resistance.Oncogene · 2025Article
- Mouse MRE11-RAD50-NBS1 is needed to start and extend meiotic DNA end resection.Nature communications · 2025Article
- Perspective in the Mechanisms for Repairing Sperm DNA Damage.Reproductive sciences (Thousand Oaks, Calif.) · 2025Review
- METTL16 is Required for Meiotic Sex Chromosome Inactivation and DSB Formation and Recombination during Male Meiosis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- EZH1/2 plays critical roles in oocyte meiosis prophase I in mice.Biological research · 2024Article
- MRE11 is essential for the long-term viability of undifferentiated spermatogonia.Cell proliferation · 2024Article
- Divergence and conservation of the meiotic recombination machinery.Nature reviews. Genetics · 2024Review
- PRAME induces genomic instability in uveal melanoma.Oncogene · 2024Article
- Genetic control of meiosis surveillance mechanisms in mammals.Frontiers in cell and developmental biology · 2023Review
- Multiple 9-1-1 complexes promote homolog synapsis, DSB repair, and ATR signaling during mammalian meiosis.eLife · 2022Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
DNA double-strand breaks (DSBs) pose a serious threat to genomic stability. Paradoxically, hundreds of programed DSBs are generated by SPO11 in meiotic prophase, which are exclusively repaired by homologous recombination (HR) to promote obligate crossover between homologous chromosomes. In somatic cells, MRE11-RAD50-NBS1 (MRN) complex-dependent DNA end resection is a prerequisite for HR repair, especially for DSBs that are covalently linked with proteins or chemicals. Interestingly, all meiotic DSBs are linked with SPO11 after being generated. Although MRN complex's function in meiotic DSB repair has been established in lower organisms, the role of MRN complex in mammalian meiotic DSB repair is not clear. Here, we show that MRN complex is essential for repairing meiotic SPO11-linked DSBs in male mice. In male germ cells, conditional inactivation of NBS1, a key component of MRN complex, causes dramatic reduction of DNA end resection and defective HR repair in meiotic prophase. NBS1 loss severely disrupts chromosome synapsis, generates abnormal chromosome structures, and eventually leads to meiotic arrest and male infertility in mice. Unlike in somatic cells, the recruitment of NBS1 to SPO11-linked DSB sites is MDC1-independent but requires other phosphorylated proteins. Collectively, our study not only reveals the significance of MRN complex in repairing meiotic DSBs but also discovers a unique mechanism that recruits MRN complex to SPO11-linked DSB sites.
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