Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

The DNA Replication Fork01:02

The DNA Replication Fork

36.6K
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...
36.6K
DNA Damage can Stall the Cell Cycle02:37

DNA Damage can Stall the Cell Cycle

9.3K
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...
9.3K
Replication in Eukaryotes01:29

Replication in Eukaryotes

14.2K
In eukaryotic cells, DNA replication is highly conserved and tightly regulated. Multiple linear chromosomes must be duplicated with high fidelity before cell division, so there are many proteins that fulfill specialized roles in the replication process. Replication occurs in three phases: initiation, elongation, and termination, and ends with two complete sets of chromosomes in the nucleus.
Many Proteins Orchestrate Replication at the Origin
Eukaryotic replication follows many of the same...
14.2K
Restarting Stalled Replication Forks02:37

Restarting Stalled Replication Forks

5.9K
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,...
5.9K
Homologous Recombination02:31

Homologous Recombination

50.9K
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...
50.9K
Replicative Cell Senescence02:15

Replicative Cell Senescence

3.7K
Replicative cell senescence is a property of cells that allows them to divide a finite number of times throughout the organism's lifespan while preventing excessive proliferation. Replicative senescence is associated with the gradual loss of the telomere — short, repetitive DNA sequences found at the end of the chromosomes. Telomeres are bound by a group of proteins to form a protective cap on the ends of chromosomes. Embryonic stem cells express telomerase — an enzyme that adds...
3.7K

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Topological stress regulates replication fork dynamics in unperturbed S phase.

Nature communications·2026
Same author

Condensin I but not Condensin II is crucial for mitotic chromosome mechanics.

Nature communications·2026
Same author

CDK12/CDK13 inhibition disrupts transcriptional elongation and replication fork progression in glioblastoma.

EMBO molecular medicine·2026
Same author

Mechanistic basis for relaxation of DNA supercoils by human topoisomerase IIIα-RMI1-RMI2.

Proceedings of the National Academy of Sciences of the United States of America·2026
Same author

OCT4 enhances the firing efficiency of late DNA replication origins in mouse embryonic stem cells.

Nature communications·2026
Same author

The SMC5/SMC6 complex is critical for resolving R-loop-induced transcription-replication conflicts.

Nucleic acids research·2026

Related Experiment Video

Updated: Aug 31, 2025

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

40.0K

RAD51 protects human cells from transcription-replication conflicts.

Rahul Bhowmick1, Mads Lerdrup1, Sampath Amitash Gadi1

  • 1Center for Chromosome Stability, Center for Healthy Aging, Department of Cellular and Molecular Medicine, University of Copenhagen, Blegdamsvej 3B, 2200 Copenhagen N, Denmark.

Molecular Cell
|August 24, 2022
PubMed
Summary

RAD51 protein prevents DNA replication fork breakage caused by transcription-replication conflicts (TRCs). Inhibiting early transcription ameliorates RAD51 depletion effects, suggesting RAD51 suppresses amplification of cancer-associated genomic loci.

Keywords:
common fragile sitesgene amplification in cancermitotic DNA synthesisoncogene-induced DNA replication stressreplication fork protection

More Related Videos

Author Spotlight: Unveiling the Role of SNF2L in Replication Fork Stability and Genome Duplication
05:55

Author Spotlight: Unveiling the Role of SNF2L in Replication Fork Stability and Genome Duplication

Published on: August 23, 2024

626
Quantifying Replication Stress in Ovarian Cancer Cells Using Single-Stranded DNA Immunofluorescence
06:25

Quantifying Replication Stress in Ovarian Cancer Cells Using Single-Stranded DNA Immunofluorescence

Published on: February 10, 2023

2.1K

Related Experiment Videos

Last Updated: Aug 31, 2025

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

40.0K
Author Spotlight: Unveiling the Role of SNF2L in Replication Fork Stability and Genome Duplication
05:55

Author Spotlight: Unveiling the Role of SNF2L in Replication Fork Stability and Genome Duplication

Published on: August 23, 2024

626
Quantifying Replication Stress in Ovarian Cancer Cells Using Single-Stranded DNA Immunofluorescence
06:25

Quantifying Replication Stress in Ovarian Cancer Cells Using Single-Stranded DNA Immunofluorescence

Published on: February 10, 2023

2.1K

Area of Science:

  • Molecular Biology
  • Cancer Biology
  • Genetics

Background:

  • Oncogene activation in cancer leads to DNA replication stress (RS) and chromosomal rearrangements.
  • Replication stress often results from conflicts between DNA replication and transcription machinery.
  • RAD51 recombinase is known to protect replication forks during RS.

Purpose of the Study:

  • To investigate the role of RAD51 in preventing transcription-replication conflicts (TRCs).
  • To identify genomic regions affected by RAD51 deficiency and their link to cancer.
  • To understand how RAD51 influences chromosomal instability.

Main Methods:

  • Studied RAD51 function in human cells.
  • Analyzed genomic regions affected by RAD51 deficiency.
  • Investigated the impact of inhibiting early S-phase transcription on RAD51-depleted cells.

Main Results:

  • RAD51 deficiency leads to replication fork breakage at TRC sites.
  • Genomic regions affected by RAD51 loss are early replicating and transcribed, overlapping with cancer amplification loci.
  • Inhibiting early S-phase transcription partially rescues adverse effects of RAD51 depletion.

Conclusions:

  • RAD51 plays a crucial role in preventing replication fork breakage during TRCs.
  • RAD51 suppresses the amplification of genomic loci susceptible to TRCs.
  • Targeting early transcription may offer therapeutic strategies for cancers with RAD51 dysfunction.