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Epigenetic Regulation

Epigenetic Regulation

Epigenetic changes alter the physical structure of the DNA without changing the genetic sequence and often regulate whether genes are turned on or off. This regulation ensures that each cell produces only proteins necessary for its function. For example, proteins that promote bone growth are not produced in muscle cells. Epigenetic mechanisms play an essential role in healthy development. Conversely, precisely regulated epigenetic mechanisms are disrupted in diseases like cancer.
X-chromosome...

Epigenetic Regulation

Epigenetic Regulation

Epigenetic mechanisms play an essential role in healthy development. Conversely, precisely regulated epigenetic mechanisms are disrupted in diseases like cancer.

Epigenetic Regulation

Epigenetic Regulation

Epigenetic mechanisms play an essential role in healthy development. Conversely, precisely regulated epigenetic mechanisms are disrupted in diseases like cancer.

Duplication of Chromatin Structure

Duplication of Chromatin Structure

The process of chromosome duplication during cell division requires genome-wide disruption and re-assembly of chromatin. The chromatin structure must be accurately inherited, reassembled, and maintained in the daughter cells to ensure lineage propagation.
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Histone Variants at the Centromere

Histone Variants at the Centromere

Histone variants are the histone proteins with structural and sequence variations. These variants may be regarded as “mutant” forms that replace their canonical histone counterparts in the nucleosomes. Specific post-translational modifications on the histone variants enable further chromatin complexity and regulate tissue-specific gene expression. The most common histone variants are from histone H2A, H2B, and linker histone H1 families. However, several variants of histone H3 variants are also...

Restarting Stalled Replication Forks

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DNA replication is initiated at sites containing predefined DNA sequences known as origins of replication. DNA is unwound at these sites by the minichromosome maintenance (MCM) helicase and other factors such as Cdc45 and the associated GINS complex.The unwound single strands are protected by replication protein A (RPA) until DNA polymerase starts synthesizing DNA at the 5’ end of the strand in the same direction as the replication fork. To prevent the replication fork from falling apart, a...

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Related Experiment Video

Updated: May 28, 2026

Single-Molecule Fluorescence Visualization of DNA Polymerase Dynamics at G-Quadruplexes

Single-Molecule Fluorescence Visualization of DNA Polymerase Dynamics at G-Quadruplexes

Published on: April 4, 2025

FANCJ coordinates two pathways that maintain epigenetic stability at G-quadruplex DNA.

Peter Sarkies¹, Pierre Murat, Lara G Phillips

¹Medical Research Council Laboratory of Molecular Biology, Hills Road, Cambridge CB2 0QH, UK.

Nucleic Acids Research

|October 25, 2011

Summary

Replication of G-quadruplex (G4) DNA is crucial for maintaining epigenetic stability. Loss of this process can lead to gene deactivation and epigenetic instability, impacting gene expression.

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Single-molecule Manipulation of G-quadruplexes by Magnetic Tweezers

Single-molecule Manipulation of G-quadruplexes by Magnetic Tweezers

Published on: September 19, 2017

Area of Science:

Molecular Biology
Genetics
Epigenetics

Background:

REV1 deficiency impairs G-quadruplex (G4) DNA replication, uncoupling DNA synthesis from histone redeposition.
This uncoupling disrupts transcriptional repression by preventing the recycling of repressive histone modifications.
Similar processes can deactivate transcriptionally active genes.

Purpose of the Study:

To investigate the impact of G4 DNA replication defects on active gene transcription.
To develop a single-cell assay for monitoring G4 DNA-associated epigenetic instability.
To elucidate the roles of FANCJ, WRN, and BLM helicases in maintaining epigenetic stability near G4 motifs.

Main Methods:

Utilized DT40 cell lines with deficiencies in DNA replication and repair proteins.
Developed a cell surface marker assay to quantify epigenetic instability at the single-cell level.
Performed transcriptional profiling to assess gene expression changes in mutant cell lines.

Main Results:

Demonstrated G4 DNA motif-associated epigenetic instability in mutants of FANCJ, WRN, and BLM helicases.
Showed that FANCJ coordinates two distinct mechanisms for maintaining epigenetic stability near G4 DNA.
Identified REV1 and the WRN/BLM helicase complex as key players in G4 replication-associated epigenetic maintenance.

Conclusions:

Efficient G4 replication in vivo requires FANCJ's 5'-3'-helicase activity, working with either a specialized polymerase or an opposing helicase.
The study provides a model for how G4 structures are replicated and how their replication impacts epigenetic stability.
The developed assay offers a sensitive tool for studying epigenetic instability in various contexts.