ArticleCell research2020
Refined spatial temporal epigenomic profiling reveals intrinsic connection between PRDM9-mediated H3K4me3 and the fate of double-stranded breaks.
Article in Cell research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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42 citing papers in PubMed, 76 citations in OpenAlex.
- Epigenetic dynamics of human spermatogenesis and their dysregulation in non-obstructive azoospermia.Protein & cell · 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
- Discovery of a potent and orally bioavailable type Ⅰ PRMTs inhibitor for triple-negative breast cancer treatment.Acta pharmacologica Sinica · 2026Article
- Partial trisomy of 1q42.1 and 8q24.3 deletion: a family history.Revista paulista de pediatria : orgao oficial da Sociedade de Pediatria de Sao Paulo · 2026Article
- The SMARCA5-DMRT1 Pioneer Complex Establishes Epigenetic Priming to Direct Male Germline Development.Research square · 2025Article
- Deciphering meiotic chromatin organization by SYCP3.Nucleic acids research · 2025Article
- Broad H3K4me3 domains orchestrate temporal control of gene expression.Cell research · 2025Article
- Paternal Exposure to Methylphenidate Induces Poor-Quality Blastocyst and Epigenetic Changes.Molecular reproduction and development · 2025Article
- SETD1B-mediated broad H3K4me3 controls proper temporal patterns of gene expression critical for spermatid development.Cell research · 2025Article
- Review
- KRAB zinc-finger proteins regulate endogenous retroviruses to sculpt germline transcriptomes and genome evolution.Genome research · 2025Article
- Epigenetic Regulation of CD8European journal of immunology · 2025Article
- Genome-wide transcriptional silencing and mRNA stabilization allow the coordinated expression of the meiotic program in mice.Nucleic acids research · 2025Article
- Dynamic changes in histone lysine lactylation during meiosis prophase I in mouse spermatogenesis.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Chromatin environment-dependent effects of DOT1L on gene expression in male germ cells.Communications biology · 2025Article
- Site-specific DNA demethylation during spermatogenesis presets the sites of nucleosome retention in mouse sperm.bioRxiv : the preprint server for biology · 2025Article
- Integrative analysis of transcriptome, DNA methylome, and chromatin accessibility reveals candidate therapeutic targets in hypertrophic cardiomyopathy.Protein & cell · 2024Article
- A Method to Study the Meiotic Recombination Map in Human Preimplantation Blastocysts.Methods in molecular biology (Clifton, N.J.) · 2024Article
- Efficient Enrichment of Synchronized Mouse Spermatocytes Suitable for Genome-Wide Analysis.Methods in molecular biology (Clifton, N.J.) · 2024Article
- Isolation of Homogeneous Sub-populations of Spermatocytes from Mouse Testis.Methods in molecular biology (Clifton, N.J.) · 2024Article
Corrections and comments
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Authors and funding
12 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Meiotic recombination is initiated by the formation of double-strand breaks (DSBs), which are repaired as either crossovers (COs) or noncrossovers (NCOs). In most mammals, PRDM9-mediated H3K4me3 controls the nonrandom distribution of DSBs; however, both the timing and mechanism of DSB fate control remain largely undetermined. Here, we generated comprehensive epigenomic profiles of synchronized mouse spermatogenic cells during meiotic prophase I, revealing spatiotemporal and functional relationships between epigenetic factors and meiotic recombination. We find that PRDM9-mediated H3K4me3 at DSB hotspots, coinciding with H3K27ac and H3K36me3, is intimately connected with the fate of the DSB. Our data suggest that the fate decision is likely made at the time of DSB formation: earlier formed DSBs occupy more open chromatins and are much more competent to proceed to a CO fate. Our work highlights an intrinsic connection between PRDM9-mediated H3K4me3 and the fate decision of DSBs, and provides new insight into the control of CO homeostasis.
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