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

Overview of DNA Repair02:25

Overview of DNA Repair

32.1K
In order to be passed through generations, genomic DNA must be undamaged and error-free. However, every day, DNA in a cell undergoes several thousand to a million damaging events by natural causes and external factors. Ionizing radiation such as UV rays, free radicals produced during cellular respiration, and hydrolytic damage from metabolic reactions can alter the structure of DNA. Damages caused include single-base alteration, base dimerization, chain breaks, and cross-linkage.
Chemically...
32.1K
Nucleotide Excision Repair01:38

Nucleotide Excision Repair

4.0K
DNA Distortion and Damage
Cells are regularly exposed to mutagens—factors in the environment that can damage DNA and generate mutations. UV radiation is one of the most common mutagens and is estimated to introduce a significant number of changes in DNA. These include bends or kinks in the structure, which can block DNA replication or transcription. If these errors are not fixed, the damage can cause mutations, which in turn can result in cancer or disease depending on which sequences are...
4.0K
DNA Damage can Stall the Cell Cycle02:37

DNA Damage can Stall the Cell Cycle

9.5K
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...
9.5K
DNA Damage Can Stall the Cell Cycle02:37

DNA Damage Can Stall the Cell Cycle

2.8K
2.8K
Base Excision Repair01:54

Base Excision Repair

23.5K
One of the common DNA damages is the chemical alteration of single bases by alkylation, oxidation, or deamination. The altered bases cause mispairing and strand breakage during replication. This type of damage causes minimal change to the DNA double helix structure and can be repaired by the base excision repair (BER) pathways. BER corrects damaged DNA sequences by removing the damaged base and restoring the original base sequence using the complementary strand as a template.
The first step of...
23.5K
Nucleosome Remodeling02:54

Nucleosome Remodeling

9.9K
Nucleosomes are the basic units of chromatin compaction. Each nucleosome consists of the DNA bound tightly around a histone core, which makes the DNA inaccessible to DNA binding proteins such as DNA polymerase and RNA polymerase. Hence, the fundamental problem is to ensure access to DNA when appropriate, despite the compact and protective chromatin structure.
Nucleosome remodeling complex
Eukaryotic cells have specialized enzymes called ATP-dependent nucleosome remodeling enzymes. These enzymes...
9.9K

You might also read

Related Articles

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

Sort by
Same author

A non-catalytic function for RAD18 in sustaining glioblastoma proliferation.

Cell reports·2026
Same author

Molecular and phenotypic blueprint of human hematopoiesis links proliferation stress to stem cell aging.

The Journal of experimental medicine·2025
Same author

TopBP1 biomolecular condensates as a new therapeutic target in advanced-stage colorectal cancer.

eLife·2025
Same author

Derivation of AZD5335, a Novel FRα-Targeted TOP1i-Loaded ADC, for the Treatment of FRα-Expressing Cancers.

Clinical cancer research : an official journal of the American Association for Cancer Research·2025
Same author

High throughput cell mechanotyping of cell response to cytoskeletal modulations using a microfluidic cell deformation system.

Microfluidics and nanofluidics·2025
Same author

Development of Low-Nanomolar Covalent Epoxide Inhibitors of Tubulin Detyrosinating Enzymes VASH1&2.

Journal of medicinal chemistry·2025

Related Experiment Video

Updated: Oct 13, 2025

Author Spotlight: Understanding DNA Damage Response in Mammalian Oocytes and Preimplantation Embryos
07:46

Author Spotlight: Understanding DNA Damage Response in Mammalian Oocytes and Preimplantation Embryos

Published on: June 23, 2023

2.8K

Studying the DNA damage response in embryonic systems.

Elena Lo Furno1, Bénédicte Recolin1, Siem van der Laan1

  • 1Institut de Génétique Humaine, Université de Montpellier, Genome Surveillance and Stability, CNRS-UMR9002, Montpellier, France.

Methods in Enzymology
|November 15, 2021
PubMed
Summary

Early embryos maintain genome integrity despite relaxed controls, crucial for preventing disease and cancer. This study details methods to investigate DNA damage response in Xenopus embryos and mouse stem cells.

Keywords:
ChromatinDNA damageDNA replicationMMSMouse embryonic stem cellsNucleusUVXenopus

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

3.7K
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

9.3K

Related Experiment Videos

Last Updated: Oct 13, 2025

Author Spotlight: Understanding DNA Damage Response in Mammalian Oocytes and Preimplantation Embryos
07:46

Author Spotlight: Understanding DNA Damage Response in Mammalian Oocytes and Preimplantation Embryos

Published on: June 23, 2023

2.8K
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

3.7K
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

9.3K

Area of Science:

  • Developmental Biology
  • Genetics
  • Cell Biology

Background:

  • Genome integrity is vital during early embryonic development to prevent mutations that can lead to diseases like cancer.
  • Early embryos exhibit relaxed genome integrity control, similar to cancer cells, posing a paradox for healthy development.

Purpose of the Study:

  • To describe protocols for studying DNA damage response and genome integrity in embryonic systems.
  • To investigate how embryos maintain genome integrity despite apparent relaxed controls.

Main Methods:

  • Utilizing early Xenopus laevis embryos and mouse embryonic stem cells (mESCs) as experimental models.
  • Employing mRNA microinjection in Xenopus embryos for gene function studies in DNA damage response.
  • Implementing cell cycle synchronization in mESCs for detailed analysis of DNA damage response.

Main Results:

  • Established methods for analyzing DNA damage response and gene functions in Xenopus embryos.
  • Developed protocols for studying DNA damage response across different cell cycle stages in mESCs.
  • Provided a framework for comparative analysis of genome integrity mechanisms.

Conclusions:

  • The described methods facilitate the study of crucial DNA damage response pathways in early development.
  • Understanding embryonic genome integrity mechanisms may illuminate dysregulation in cancer cells.
  • This research contributes to deciphering how healthy individuals develop under conditions of relaxed genome surveillance.