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Related Concept Videos

Restarting Stalled Replication Forks02:37

Restarting Stalled Replication Forks

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...
Restarting Stalled Replication Forks02:37

Restarting Stalled Replication Forks

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...
The DNA Replication Fork01:02

The DNA Replication Fork

An organism’s genome needs to be duplicated in an efficient and error-free manner for its growth and survival. The replication fork is a Y-shaped active region where two strands of DNA are separated and replicated continuously. The coupling of DNA unzipping and complementary strand synthesis is a characteristic feature of a replication fork.   Organisms with small circular DNA, such as E. coli, often have a single origin of replication; therefore, they have only two replication forks, one in...
The DNA Replication Fork01:02

The DNA Replication Fork

An organism’s genome needs to be duplicated in an efficient and error-free manner for its growth and survival. The replication fork is a Y-shaped active region where two strands of DNA are separated and replicated continuously. The coupling of DNA unzipping and complementary strand synthesis is a characteristic feature of a replication fork.   Organisms with small circular DNA, such as E. coli, often have a single origin of replication; therefore, they have only two replication forks, one in...
DNA Damage can Stall the Cell Cycle02:36

DNA Damage can Stall the Cell Cycle

In response to DNA damage, cells can pause the cell cycle to assess and repair the breaks. However, the cell must check the DNA at certain critical stages during the cell cycle. If the cell cycle pauses before DNA replication, the cells will contain twice the amount of DNA. On the other hand, if cells arrest after DNA replication but before mitosis, they will contain four times the normal amount of DNA. With a host of specialized proteins at their disposal,cells must use the right protein at...
DNA Damage Can Stall the Cell Cycle02:36

DNA Damage Can Stall the Cell Cycle

In response to DNA damage, cells can pause the cell cycle to assess and repair the breaks. However, the cell must check the DNA at certain critical stages during the cell cycle. If the cell cycle pauses before DNA replication, the cells will contain twice the amount of DNA. On the other hand, if cells arrest after DNA replication but before mitosis, they will contain four times the normal amount of DNA. With a host of specialized proteins at their disposal,cells must use the right protein at...

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Related Experiment Video

Updated: Jul 3, 2026

Direct Restart of a Replication Fork Stalled by a Head-On RNA Polymerase
07:27

Direct Restart of a Replication Fork Stalled by a Head-On RNA Polymerase

Published on: April 29, 2010

Replication-stress-induced chromatin loops protect fork stability.

Vincent Gaggioli1,2, Kaustav Sengupta1,2,3, Ashutosh Choudhury1,2

  • 1Department of Molecular Genetics, Erasmus University Medical Center, Erasmus MC Cancer Institute, Rotterdam, the Netherlands.

Nature
|July 1, 2026
PubMed
Summary
This summary is machine-generated.

Replication stress forms protective chromatin loops around stalled forks, shielding them from degradation. This 3D genome organization is crucial for maintaining genome integrity and preventing mutations.

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Inducing a Site Specific Replication Blockage in E. coli Using a Fluorescent Repressor Operator System
11:19

Inducing a Site Specific Replication Blockage in E. coli Using a Fluorescent Repressor Operator System

Published on: August 21, 2016

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

Published on: January 14, 2016

Related Experiment Videos

Last Updated: Jul 3, 2026

Direct Restart of a Replication Fork Stalled by a Head-On RNA Polymerase
07:27

Direct Restart of a Replication Fork Stalled by a Head-On RNA Polymerase

Published on: April 29, 2010

Inducing a Site Specific Replication Blockage in E. coli Using a Fluorescent Repressor Operator System
11:19

Inducing a Site Specific Replication Blockage in E. coli Using a Fluorescent Repressor Operator System

Published on: August 21, 2016

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

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

Published on: January 14, 2016

Area of Science:

  • Genomics
  • Molecular Biology
  • Epigenetics

Background:

  • Replication stress threatens genome integrity.
  • The role of higher-order chromatin organization in replication fork protection is not well understood.

Purpose of the Study:

  • To investigate how chromatin organization protects replication forks during stress.
  • To elucidate the mechanisms of replication fork stabilization.

Main Methods:

  • Analysis of chromatin loops formation under replication stress.
  • Investigating the role of CTCF and G9a in loop stabilization.
  • Assessing the impact of loop destabilization on nascent DNA degradation.

Main Results:

  • Replication stress induces transient chromatin loops enclosing stalled forks.
  • CTCF and G9a-dependent heterochromatin stabilize these loops.
  • Loss of loop stability leads to nascent-strand degradation and increased mutation susceptibility.
  • This architecture is critical in BRCA2-deficient cells.

Conclusions:

  • Replication-stress-induced 3D genome reorganization is fundamental for replication fork stability.
  • This process mitigates mutagenesis and genomic instability.