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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 1, 2026

Detection of Post-Replicative Gaps Accumulation and Repair in Human Cells Using the DNA Fiber Assay
10:32

Detection of Post-Replicative Gaps Accumulation and Repair in Human Cells Using the DNA Fiber Assay

Published on: February 3, 2022

Fanconi anemia proteins stabilize replication forks.

Lily Chien Wang1, Stacie Stone, Maureen Elizabeth Hoatlin

  • 1Institute for Cancer Genetics, Columbia University, New York, NY 10032, USA.

DNA Repair
|September 13, 2008
PubMed
Summary

Fanconi anemia proteins are crucial for restarting DNA replication after damage. FANCL depletion impairs this process, highlighting the FA pathway

Area of Science:

  • Molecular Biology
  • Genetics
  • Cell Biology

Background:

  • Fanconi anemia (FA) is a genetic disorder linked to DNA repair and replication defects.
  • The FA core complex and FANCD2 protein associate with chromatin during DNA replication.
  • The precise function of FA proteins during DNA replication remains unclear.

Purpose of the Study:

  • To investigate the role of Fanconi anemia proteins in DNA replication restart and repair.
  • To elucidate the mechanism of FA protein involvement at replication forks.

Main Methods:

  • Utilized Xenopus cell-free extracts to study DNA replication dynamics.
  • Depleted FANCL protein to assess its impact on replication restart.
  • Treated cells with camptothecin and mitomycin C to induce DNA damage.

More Related Videos

Visualization of DNA Replication in the Vertebrate Model System DT40 using the DNA Fiber Technique
07:18

Visualization of DNA Replication in the Vertebrate Model System DT40 using the DNA Fiber Technique

Published on: October 27, 2011

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

Related Experiment Videos

Last Updated: Jul 1, 2026

Detection of Post-Replicative Gaps Accumulation and Repair in Human Cells Using the DNA Fiber Assay
10:32

Detection of Post-Replicative Gaps Accumulation and Repair in Human Cells Using the DNA Fiber Assay

Published on: February 3, 2022

Visualization of DNA Replication in the Vertebrate Model System DT40 using the DNA Fiber Technique
07:18

Visualization of DNA Replication in the Vertebrate Model System DT40 using the DNA Fiber Technique

Published on: October 27, 2011

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

Main Results:

  • FANCL depletion led to defective DNA replication restart after camptothecin treatment.
  • This defect was more severe after mitomycin C treatment, suggesting a role in crosslink repair.
  • FA core complex binding to chromatin during replication follows origin firing and requires RPA.
  • FANCD2 chromatin binding additionally depends on ATR, indicating roles at replication forks.

Conclusions:

  • FA proteins are essential for replication restart at collapsed replication forks.
  • The FA pathway plays a significant role in managing DNA replication stress and damage.