ArticleGenome research2017
In vivo binding of PRDM9 reveals interactions with noncanonical genomic sites.
Article in Genome research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 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
46 citing papers in PubMed, 82 citations in OpenAlex.
- PRDM9-mediated meiotic hotspot specification is constrained in humans despite extensive sequence diversity.bioRxiv : the preprint server for biology · 2026Article
- High-resolution chromatin mapping reveals that CTCF anchors meiotic loops to the chromosome axis.Nature communications · 2026Article
- Why recombination hotspots?PLoS genetics · 2026Review
- Independent genetic basis of meiotic crossover positioning and interference in domestic pigs.Scientific reports · 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
- Crossing epigenetic frontiers: the intersection of novel histone modifications and diseases.Signal transduction and targeted therapy · 2024Review
- FIGNL1-FIRRM is essential for meiotic recombination and prevents DNA damage-independent RAD51 and DMC1 loading.Nature communications · 2024Article
- Bridging the gap between the evolutionary dynamics and the molecular mechanisms of meiosis: A model based exploration of the PRDM9 intra-genomic Red Queen.PLoS genetics · 2024Article
- Chromatin remodeler CHD8 is required for spermatogonial proliferation and early meiotic progression.Nucleic acids research · 2024Article
- Down the Penrose stairs, or how selection for fewer recombination hotspots maintains their existence.eLife · 2023Article
- The RNA-binding protein FUS/TLS interacts with SPO11 and PRDM9 and localize at meiotic recombination hotspots.Cellular and molecular life sciences : CMLS · 2023Article
- TOPOVIBL-REC114 interaction regulates meiotic DNA double-strand breaks.Nature communications · 2022Article
- The histone modification reader ZCWPW1 promotes double-strand break repair by regulating cross-talk of histone modifications and chromatin accessibility at meiotic hotspots.Genome biology · 2022Article
- Histone post-translational modifications - cause and consequence of genome function.Nature reviews. Genetics · 2022Review
- Genome-wide variability in recombination activity is associated with meiotic chromatin organization.Genome research · 2021Article
- Evolution of Recombination Landscapes in Diverging Populations of Bread Wheat.Genome biology and evolution · 2021Article
- Rat PRDM9 shapes recombination landscapes, duration of meiosis, gametogenesis, and age of fertility.BMC biology · 2021Article
- Chromosome-wide characterization of meiotic noncrossovers (gene conversions) in mouse hybrids.Genetics · 2021Article
- Article
- Meiotic cohesins mediate initial loading of HORMAD1 to the chromosomes and coordinate SC formation during meiotic prophase.PLoS genetics · 2020Article
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In mouse and human meiosis, DNA double-strand breaks (DSBs) initiate homologous recombination and occur at specific sites called hotspots. The localization of these sites is determined by the sequence-specific DNA binding domain of the PRDM9 histone methyl transferase. Here, we performed an extensive analysis of PRDM9 binding in mouse spermatocytes. Unexpectedly, we identified a noncanonical recruitment of PRDM9 to sites that lack recombination activity and the PRDM9 binding consensus motif. These sites include gene promoters, where PRDM9 is recruited in a DSB-dependent manner. Another subset reveals DSB-independent interactions between PRDM9 and genomic sites, such as the binding sites for the insulator protein CTCF. We propose that these DSB-independent sites result from interactions between hotspot-bound PRDM9 and genomic sequences located on the chromosome axis.
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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.