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

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...
Homologous Recombination02:31

Homologous Recombination

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...
Fixing Double-strand Breaks02:04

Fixing Double-strand Breaks

The double-stranded structure of DNA has two major advantages. First, it serves as a safe repository of genetic information where one strand serves as the back-up in case the other strand is damaged. Second, the double-helical structure can be wrapped around proteins called histones to form nucleosomes, which can then be tightly wound to form chromosomes. This way, DNA chains up to 2 inches long can be contained within microscopic structures in a cell. A double-stranded break not only damages...
Fixing Double-strand Breaks02:04

Fixing Double-strand Breaks

The double-stranded structure of DNA has two major advantages. First, it serves as a safe repository of genetic information where one strand serves as the back-up in case the other strand is damaged. Second, the double-helical structure can be wrapped around proteins called histones to form nucleosomes, which can then be tightly wound to form chromosomes. This way, DNA chains up to 2 inches long can be contained within microscopic structures in a cell. A double-stranded break not only damages...
Meiosis vs. Mitosis02:57

Meiosis vs. Mitosis

Cell division is necessary for growth and reproduction in organisms. Mitosis aids cell growth and development by dividing somatic cells. In contrast, meiosis causes the division of germ cells and plays an essential role in sexual reproduction. Due to their unique functional requirements, mitosis and meiosis differ from each other in multiple aspects.
Before the start of mitosis and meiosis I, the cell synthesizes DNA, resulting in two homologous copies of each chromosome. DNA synthesis is...

You might also read

Related Articles

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

Sort by
Same author

K63-linked ubiquitylation of S2P-RNAPII regulates transcription in a DNAPK inter-dependent manner in response to double-strand breaks.

Nucleic acids research·2026
Same author

Mature Tertiary Lymphoid Structures in Breast Cancers Are Associated With Antitumor Immunity and Better Prognosis.

Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc·2026
Same author

Programmed Death Ligand-1 Testing in Triple-Negative Breast Cancer: National Practice and Interlaboratory Variation in the Netherlands.

Laboratory investigation; a journal of technical methods and pathology·2026
Same author

Association of copy number alterations with the immune transcriptomic landscape in cancer.

NPJ systems biology and applications·2026
Same author

CIP2A mediates mitotic recruitment of SLX4/MUS81/XPF to resolve replication stress-induced DNA lesions.

Nature communications·2025
Same author

WEE1 inhibitors trigger GCN2-mediated activation of the integrated stress response.

Nature communications·2025
Same journal

Monoallelic germline RAD51C, RAD51D, and BRIP1 variants in hereditary cancer testing: Variant spectrum and clinical counselling implications.

Mutation research·2026
Same journal

Prediction of hepatocellular carcinoma associated biomarkers in TP53 gene; A comprehensive in silico analysis.

Mutation research·2026
Same journal

IDH1 mutation promotes angiogenesis via upregulation of hypoxia inducible factor 1 alpha in glial tumors.

Mutation research·2026
Same journal

Targeting overexpressed oncogenes in esophageal cancer through miRNA-mediated gene silencing: Insights from binding affinity and thermodynamic profiling.

Mutation research·2026
Same journal

The active compound quercetin from Polygonum cuspidatum targets COL3A1 to enhance CD8⁺ T cell cytotoxicity in gastric cancer.

Mutation research·2026
Same journal

E2F1 promotes LIHC malignant phenotype via NEK2-mediated Wnt/β-catenin and Notch activation and EMT.

Mutation research·2026
See all related articles

Related Experiment Video

Updated: May 9, 2026

Two- and Three-Dimensional Live Cell Imaging of DNA Damage Response Proteins
10:24

Two- and Three-Dimensional Live Cell Imaging of DNA Damage Response Proteins

Published on: September 28, 2012

The DNA damage response during mitosis.

Anne Margriet Heijink1, Małgorzata Krajewska, Marcel A T M van Vugt

  • 1Department of Medical Oncology, University Medical Centre Groningen, University of Groningen, Hanzeplein 1, 9723GZ Groningen, The Netherlands.

Mutation Research
|July 25, 2013
PubMed
Summary
This summary is machine-generated.

Cells manage DNA damage using the DNA damage response (DDR) network. During mitosis, DDR signaling is rewired, delaying repair until after cell division, which is crucial for cancer therapy.

Keywords:
AdaptationCell cycleCheckpointMitosisMutagenesisRecovery

More Related Videos

Visualizing and Quantifying Endonuclease-Based Site-Specific DNA Damage
10:59

Visualizing and Quantifying Endonuclease-Based Site-Specific DNA Damage

Published on: August 21, 2021

Characterizing DNA Repair Processes at Transient and Long-lasting Double-strand DNA Breaks by Immunofluorescence Microscopy
08:31

Characterizing DNA Repair Processes at Transient and Long-lasting Double-strand DNA Breaks by Immunofluorescence Microscopy

Published on: June 8, 2018

Related Experiment Videos

Last Updated: May 9, 2026

Two- and Three-Dimensional Live Cell Imaging of DNA Damage Response Proteins
10:24

Two- and Three-Dimensional Live Cell Imaging of DNA Damage Response Proteins

Published on: September 28, 2012

Visualizing and Quantifying Endonuclease-Based Site-Specific DNA Damage
10:59

Visualizing and Quantifying Endonuclease-Based Site-Specific DNA Damage

Published on: August 21, 2021

Characterizing DNA Repair Processes at Transient and Long-lasting Double-strand DNA Breaks by Immunofluorescence Microscopy
08:31

Characterizing DNA Repair Processes at Transient and Long-lasting Double-strand DNA Breaks by Immunofluorescence Microscopy

Published on: June 8, 2018

Area of Science:

  • Cellular biology
  • Molecular oncology
  • DNA repair mechanisms

Background:

  • The DNA damage response (DDR) network is crucial for recognizing DNA lesions and initiating repair or cell death pathways.
  • DDR signaling varies across the cell cycle, with diminished responses observed during mitosis, particularly for DNA double-strand breaks.
  • Previous studies noted that cells irradiated during mitosis divide with unrepaired chromosomes, indicating altered DDR activity.

Purpose of the Study:

  • To elucidate the molecular mechanisms underlying DDR signaling rewiring during mitosis.
  • To understand how cells handle DNA damage encountered specifically during the mitotic phase.
  • To explore the implications of mitotic DDR modulation for cancer treatment strategies.

Main Methods:

  • Review of existing literature on DDR signaling pathways.
  • Analysis of molecular mechanisms that regulate DDR during cell division.
  • Discussion of cellular fate consequences following mitotic DNA damage.

Main Results:

  • Mitosis involves specific inactivation of certain DDR signaling pathways, rather than a complete shutdown.
  • Cells appear to "mark" DNA damage during mitosis for subsequent repair after exiting this phase.
  • Understanding these mitotic adaptations is key to cancer therapy involving DNA-damaging agents and mitotic inhibitors.

Conclusions:

  • Mitotic DDR is actively modulated, not simply absent, allowing for post-mitotic repair.
  • Cancer cells' handling of DNA damage during interphase versus mitosis presents therapeutic vulnerabilities.
  • Further research into mitotic DDR is essential for developing more effective cancer treatments.