ArticleNucleic acids research2021
Four-pronged negative feedback of DSB machinery in meiotic DNA-break control in mice.
Article in Nucleic acids research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
20 citing papers in PubMed, 38 citations in OpenAlex.
- SYCP2 recruits HORMAD2 to chromosome axes for unsynapsed chromatin silencing and synapsis surveillance in meiosis.Nature communications · 2026Article
- Mei4 deficiency induces sexual dimorphism in early meiosis and promotes production of unreduced eggs in zebrafish.Zoological research · 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
- BAF-1-VRK-1 mediated release of meiotic chromosomes from the nuclear periphery is important for genome integrity.Nature communications · 2025Article
- Biochemical Mechanisms of Genetic Recombination and DNA Repair.Annual review of biochemistry · 2025Review
- Keeping it safe: control of meiotic chromosome breakage.Trends in genetics : TIG · 2025Review
- Genome-wide transcriptional silencing and mRNA stabilization allow the coordinated expression of the meiotic program in mice.Nucleic acids research · 2025Article
- Bi-allelic missense variants in MEI4 cause preimplantation embryonic arrest and female infertility.Human genetics · 2024Article
- Seeding the meiotic DNA break machinery and initiating recombination on chromosome axes.Nature communications · 2024Article
- Characterization of the REC114-MEI4-IHO1 complex regulating meiotic DNA double-strand break formation.The EMBO journal · 2023Article
- DNA double-strand break genetic variants in patients with premature ovarian insufficiency.Journal of ovarian research · 2023Review
- TOPOVIBL-REC114 interaction regulates meiotic DNA double-strand breaks.Nature communications · 2022Article
- Article
- Chromosomal synapsis defects can trigger oocyte apoptosis without elevating numbers of persistent DNA breaks above wild-type levels.Nucleic acids research · 2022Article
- Conservation and divergence of meiotic DNA double strand break forming mechanisms in Arabidopsis thaliana.Nucleic acids research · 2021Article
- Sycp1 Is Not Required for Subtelomeric DNA Double-Strand Breaks but Is Required for Homologous Alignment in Zebrafish Spermatocytes.Frontiers in cell and developmental biology · 2021Article
- Meiotic Chromosome Dynamics in Zebrafish.Frontiers in cell and developmental biology · 2021Review
- Meiotic Crossover Patterning.Frontiers in cell and developmental biology · 2021Review
- Chromosome Organization in Early Meiotic Prophase.Frontiers in cell and developmental biology · 2021Review
- The formation and repair of DNA double-strand breaks in mammalian meiosis.Asian journal of andrologyReview
Corrections and comments
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Authors and funding
13 authors at 6 institutions in 5 countries.
Funding
Abstract
In most taxa, halving of chromosome numbers during meiosis requires that homologous chromosomes (homologues) pair and form crossovers. Crossovers emerge from the recombination-mediated repair of programmed DNA double-strand breaks (DSBs). DSBs are generated by SPO11, whose activity requires auxiliary protein complexes, called pre-DSB recombinosomes. To elucidate the spatiotemporal control of the DSB machinery, we focused on an essential SPO11 auxiliary protein, IHO1, which serves as the main anchor for pre-DSB recombinosomes on chromosome cores, called axes. We discovered that DSBs restrict the DSB machinery by at least four distinct pathways in mice. Firstly, by activating the DNA damage response (DDR) kinase ATM, DSBs restrict pre-DSB recombinosome numbers without affecting IHO1. Secondly, in their vicinity, DSBs trigger IHO1 depletion mainly by another DDR kinase, ATR. Thirdly, DSBs enable homologue synapsis, which promotes the depletion of IHO1 and pre-DSB recombinosomes from synapsed axes. Finally, DSBs and three DDR kinases, ATM, ATR and PRKDC, enable stage-specific depletion of IHO1 from all axes. We hypothesize that these four negative feedback pathways protect genome integrity by ensuring that DSBs form without excess, are well-distributed, and are restricted to genomic locations and prophase stages where DSBs are functional for promoting homologue pairing and crossover formation.
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Registered trials
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.