ArticleScientific reports2016
Chromatin architecture may dictate the target site for DMC1, but not for RAD51, during homologous pairing.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 14 citations in OpenAlex.
- On the origin of PRDM9-guided recombination hotspots.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Functional dissection of complex and molecular trait variants at single nucleotide resolution.bioRxiv : the preprint server for biology · 2024Article
- Molecular structures and mechanisms of DNA break processing in mouse meiosis.Genes & development · 2020Article
- The intrinsic ability of double-stranded DNA to carry out D-loop and R-loop formation.Computational and structural biotechnology journal · 2020Review
- Molecular evolution of the meiotic recombination pathway in mammals.Evolution; international journal of organic evolution · 2019Article
- Factors influencing meiotic recombination revealed by whole-genome sequencing of single sperm.Science (New York, N.Y.) · 2019Article
- BRDT is an essential epigenetic regulator for proper chromatin organization, silencing of sex chromosomes and crossover formation in male meiosis.PLoS genetics · 2018Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
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Abstract
In eukaryotes, genomic DNA is compacted as chromatin, in which histones and DNA form the nucleosome as the basic unit. DMC1 and RAD51 are essential eukaryotic recombinases that mediate homologous chromosome pairing during homologous recombination. However, the means by which these two recombinases distinctly function in chromatin have remained elusive. Here we found that, in chromatin, the human DMC1-single-stranded DNA complex bypasses binding to the nucleosome, and preferentially promotes homologous pairing at the nucleosome-depleted regions. Consistently, DMC1 forms ternary complex recombination intermediates with the nucleosome-free DNA or the nucleosome-depleted DNA region. Surprisingly, removal of the histone tails improperly enhances the nucleosome binding by DMC1. In contrast, RAD51 does not specifically target the nucleosome-depleted region in chromatin. These are the first demonstrations that the chromatin architecture specifies the sites to promote the homologous recombination reaction by DMC1, but not by RAD51.
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