ArticleThe Journal of biological chemistry2009
Evidence that nucleosomes inhibit mismatch repair in eukaryotic cells.
Article in The Journal of biological chemistry, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
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Who cites it
47 citing papers in PubMed, 68 citations in OpenAlex.
- Article
- Microsatellite break-induced replication generates highly mutagenized extrachromosomal circular DNAs.NAR cancer · 2024Article
- DNA Repair in Nucleosomes: Insights from Histone Modifications and Mutants.International journal of molecular sciences · 2024Review
- Mismatch Repair Protein Msh2 Is Necessary for Macronuclear Stability and Micronuclear Division inInternational journal of molecular sciences · 2023Article
- MMR Deficiency Defines Distinct Molecular Subtype of Breast Cancer with Histone Proteomic Networks.International journal of molecular sciences · 2023Article
- Chaperoning histones at the DNA repair dance.DNA repair · 2021Review
- Review
- Mutperiod: Analysis of periodic mutation rates in nucleosomes.Computational and structural biotechnology journal · 2021Article
- DNA mismatch repair in the chromatin context: Mechanisms and therapeutic potential.DNA repair · 2020Review
- Dynamic human MutSα-MutLα complexes compact mismatched DNA.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Nucleosome positioning stability is a modulator of germline mutation rate variation across the human genome.Nature communications · 2020Article
- Chromatin remodeling and mismatch repair: Access and excision.DNA repair · 2020Review
- H3K36me3, message from chromatin to DNA damage repair.Cell & bioscience · 2020Review
- Article
- Coordinating Multi-Protein Mismatch Repair by Managing Diffusion Mechanics on the DNA.Journal of molecular biology · 2018Review
- Nucleosomes around a mismatched base pair are excluded via an Msh2-dependent reaction with the aid of SNF2 family ATPase Smarcad1.Genes & development · 2018Article
- Involvement of DNA mismatch repair in the maintenance of heterochromatic DNA stability in Saccharomyces cerevisiae.PLoS genetics · 2017Article
- Epigenetic Enhancement of the Post-replicative DNA Mismatch Repair of Mammalian Genomes by a Hemi-Scientific reports · 2016Article
- Understanding how mismatch repair proteins participate in the repair/anti-recombination decision.FEMS yeast research · 2016Article
- DNA Mismatch Repair Interacts with CAF-1- and ASF1A-H3-H4-dependent Histone (H3-H4)2 Tetramer Deposition.The Journal of biological chemistry · 2016Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
The influence of chromatin structure on DNA metabolic processes, including DNA replication and repair, has been a matter of intensive studies in recent years. Although the human mismatch repair (MMR) reaction has been reconstituted using purified proteins, the influence of chromatin structure on human MMR is unknown. This study examines the interaction between human MutSalpha and a mismatch located within a nucleosome or between two nucleosomes. The results show that, whereas MutSalpha specifically recognizes both types of nucleosomal heteroduplexes, the protein bound the mismatch within a nucleosome with much lower efficiency than a naked heteroduplex or a heterology free of histone proteins but between two nucleosomes. Additionally, MutSalpha displays reduced ATPase- and ADP-binding activity when interacting with nucleosomal heteroduplexes. Interestingly, nucleosomes block ATP-induced MutSalpha sliding along the DNA helix when the mismatch is in between two nucleosomes. These findings suggest that nucleosomes may inhibit MMR in eukaryotic cells. The implications of these findings for our understanding of eukaryotic MMR are discussed.
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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.