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Related Concept Videos

Mismatch Repair01:36

Mismatch Repair

Overview
Mismatch Repair01:20

Mismatch Repair

Organisms are capable of detecting and fixing nucleotide mismatches that occur during DNA replication. This sophisticated process requires identifying the new strand and replacing the erroneous bases with correct nucleotides. Mismatch repair is coordinated by many proteins in both prokaryotes and eukaryotes.
The Mutator Protein Family Plays a Key Role in DNA Mismatch Repair
The human genome has more than 3 billion base pairs of DNA per cell. Prior to cell division, that vast amount of genetic...
Mismatch Repair01:36

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Homologous Recombination02:31

Homologous Recombination

The basic reaction of homologous recombination (HR) involves two chromatids that contain DNA sequences sharing a significant stretch of identity. One of these sequences uses a strand from another as a template to synthesize DNA in an enzyme-catalyzed reaction. The final product is a novel amalgamation of the two substrates. To ensure an accurate recombination of sequences, HR is restricted to the S and G2 phases of the cell cycle. At these stages, the DNA has been replicated already and the...
Homologous Recombination02:31

Homologous Recombination

The basic reaction of homologous recombination (HR) involves two chromatids that contain DNA sequences sharing a significant stretch of identity. One of these sequences uses a strand from another as a template to synthesize DNA in an enzyme-catalyzed reaction. The final product is a novel amalgamation of the two substrates. To ensure an accurate recombination of sequences, HR is restricted to the S and G2 phases of the cell cycle. At these stages, the DNA has been replicated already and the...
Nucleosome Remodeling02:54

Nucleosome Remodeling

Nucleosomes are the basic units of chromatin compaction. Each nucleosome consists of the DNA bound tightly around a histone core, which makes the DNA inaccessible to DNA binding proteins such as DNA polymerase and RNA polymerase. Hence, the fundamental problem is to ensure access to DNA when appropriate, despite the compact and protective chromatin structure.
Nucleosome remodeling complex
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Related Experiment Video

Updated: May 26, 2026

Examination of Proteins Bound to Nascent DNA in Mammalian Cells Using BrdU-ChIP-Slot-Western Technique
09:14

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Published on: January 14, 2016

Interplay between mismatch repair and chromatin assembly.

Barbara Schöpf1, Stephanie Bregenhorn, Jean-Pierre Quivy

  • 1Institute of Molecular Cancer Research, University of Zurich, Winterthurerstasse 190, CH-8057 Zurich, Switzerland.

Proceedings of the National Academy of Sciences of the United States of America
|January 11, 2012
PubMed
Summary

DNA mismatches delay nucleosome loading by chromatin assembly factor 1 (CAF-1). Mismatch repair (MMR) must complete before CAF-1 can efficiently load histones, suggesting a complex interplay between DNA repair and chromatin assembly.

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Last Updated: May 26, 2026

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Published on: January 14, 2016

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06:32

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Published on: March 9, 2022

Area of Science:

  • Molecular Biology
  • Epigenetics
  • DNA Repair

Background:

  • Single-strand nicks and gaps in DNA enhance nucleosome loading by chromatin assembly factor 1 (CAF-1).
  • Mismatch repair (MMR) system utilizes these discontinuities as loading sites for exonuclease 1, initiating degradation of the error-containing strand.
  • Chromatin packaging may potentially inhibit MMR, necessitating an investigation into differential regulation of chromatin assembly on various DNA substrates.

Purpose of the Study:

  • To investigate whether chromatin assembly is differentially regulated on heteroduplex (mismatch-containing) versus homoduplex (mismatch-free) DNA substrates.
  • To elucidate the regulatory mechanisms governing the interplay between MMR and chromatin assembly.
  • To explore the role of proliferating cell nuclear antigen (PCNA) and its interactions with MMR and CAF-1 components.

Main Methods:

  • Utilized nicked plasmid substrates with and without mismatches in human cell extracts.
  • Investigated nucleosome loading efficiency in the presence of mismatches.
  • Examined interactions between MutSα, CAF-1, and PCNA using biochemical and cellular assays.
  • Assessed the impact of S-phase progression and CAF-1 p150 phosphorylation on these interactions.

Main Results:

  • The presence of a mismatch in a nicked DNA substrate significantly delays nucleosome loading by CAF-1.
  • Following mismatch removal and repair of the single-stranded gap, efficient nucleosome loading occurs.
  • MutSα and CAF-1 directly interact with each other, in addition to their individual interactions with PCNA.
  • This MutSα-CAF-1 interaction is enhanced during S-phase and potentially regulated by the phosphorylation of CAF-1's p150 subunit.

Conclusions:

  • DNA mismatch presence actively delays chromatin assembly, ensuring MMR completion before DNA packaging.
  • The interplay between MMR and chromatin assembly is complex, involving direct interactions between MutSα and CAF-1, mediated by PCNA.
  • Regulation of these interactions during S-phase, possibly through CAF-1 phosphorylation, fine-tunes the balance between DNA repair and genome organization.