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

42.1K
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...
42.1K
The DNA Replication Fork01:02

The DNA Replication Fork

19.0K
19.0K
Restarting Stalled Replication Forks02:37

Restarting Stalled Replication Forks

6.5K
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,...
6.5K
Restarting Stalled Replication Forks02:37

Restarting Stalled Replication Forks

2.4K
2.4K
DNA Damage can Stall the Cell Cycle02:36

DNA Damage can Stall the Cell Cycle

10.3K
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...
10.3K
DNA Damage Can Stall the Cell Cycle02:36

DNA Damage Can Stall the Cell Cycle

3.3K
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...
3.3K

You might also read

Related Articles

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

Sort by
Same author

SETDB1 is critically required for uveal melanoma growth and represents a promising therapeutic target.

Cell death & disease·2025
Same author

Assessing the Status of Cyclin E1 (CCNE1) From Gene to Protein Level in Ovarian and Endometrial Carcinomas: A Systematic Review.

Laboratory investigation; a journal of technical methods and pathology·2025
Same author

Editorial: DNA replication barriers and the origins of cancer.

Frontiers in cell and developmental biology·2025
Same author

The DNA Damage Response as an Auxiliary Indicator of Senescence in Cancer: A User-Friendly Toolkit of Markers and Detection Methods.

Methods in molecular biology (Clifton, N.J.)·2025
Same author

Understanding DNA replication and replication stress as avenues to combat cancer.

Communications biology·2024
Same author

Aberrant DNA repair reveals a vulnerability in histone H3.3-mutant brain tumors.

Nucleic acids research·2024

Related Experiment Video

Updated: Mar 7, 2026

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

2.5K

Rescue from replication stress during mitosis.

Michalis Fragkos1, Valeria Naim1

  • 1a CNRS UMR8200 , University Paris-Saclay , Gustave Roussy, Villejuif , France.

Cell Cycle (Georgetown, Tex.)
|February 7, 2017
PubMed
Summary

Genomic instability, a cancer hallmark, is driven by DNA replication stress. Mitotic rescue from replication stress (MRRS) pathways are crucial for genome stability, and their deregulation can lead to cancer and aging.

Keywords:
DNA replication stressanaphase bridgesfragile sitesgenomic instabilitymitosis

More Related Videos

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

14.0K
Chromosome Replicating Timing Combined with Fluorescent In situ Hybridization
17:14

Chromosome Replicating Timing Combined with Fluorescent In situ Hybridization

Published on: December 10, 2012

14.6K

Related Experiment Videos

Last Updated: Mar 7, 2026

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

2.5K
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

14.0K
Chromosome Replicating Timing Combined with Fluorescent In situ Hybridization
17:14

Chromosome Replicating Timing Combined with Fluorescent In situ Hybridization

Published on: December 10, 2012

14.6K

Area of Science:

  • Molecular Biology
  • Genetics
  • Cell Biology

Background:

  • Genomic instability is a key characteristic of cancer and various human disorders.
  • DNA replication stress is increasingly recognized as a primary driver of genomic instability and cancer development.
  • Cells possess specific pathways for resolving DNA replication stress during mitosis, termed mitotic rescue from replication stress (MRRS).

Purpose of the Study:

  • To review the causes and consequences of DNA replication stress.
  • To focus on the persistence of replication stress during mitosis.
  • To discuss the mechanisms and factors involved in resolving replication stress and its impact on health and disease.

Main Methods:

  • Literature review of recent evidence on DNA replication stress.
  • Analysis of cellular pathways involved in mitotic rescue from replication stress (MRRS).
  • Discussion of the link between aberrant MRRS and tumorigenesis, aging, and disease.

Main Results:

  • DNA replication stress is a major contributor to genomic instability and cancer.
  • Mitotic rescue from replication stress (MRRS) is essential for maintaining genome stability.
  • Dysregulation of MRRS pathways, due to oncogene activation or loss of caretaker genes, can cause chromosomal aberrations driving cancer.

Conclusions:

  • Replication stress persistence in mitosis and aberrant MRRS are implicated in cancer initiation and progression.
  • Understanding MRRS mechanisms is crucial for addressing diseases linked to genomic instability.
  • Aberrant MRRS may contribute to aging and other human disorders beyond cancer.