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

31.4K
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...
31.4K
Translesion DNA Polymerases02:10

Translesion DNA Polymerases

10.1K
Translesion (TLS) polymerases rescue stalled DNA polymerases at sites of damaged bases by replacing the replicative polymerase and installing a nucleotide across the damaged site. Doing so, TLS allows additional time for the cell to repair the damage before resuming regular DNA replication.
TLS polymerases are found in all three domains of life - archaea, bacteria, and eukaryotes. Of the different classes of TLS polymerases, members of the Y family are fitted with specialized structures that...
10.1K
Nucleotide Excision Repair01:38

Nucleotide Excision Repair

3.7K
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...
3.7K
Mismatch Repair01:20

Mismatch Repair

5.1K
Organisms are capable of detecting and fixing nucleotide mismatches that occur during DNA replication. This sophisticated process requires identifying the new strand and replacing the erroneous bases with correct nucleotides. Mismatch repair is coordinated by many proteins in both prokaryotes and eukaryotes.
The Mutator Protein Family Plays a Key Role in DNA Mismatch Repair
The human genome has more than 3 billion base pairs of DNA per cell. Prior to cell division, that vast amount of genetic...
5.1K
Fixing Double-strand Breaks02:04

Fixing Double-strand Breaks

12.8K
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...
12.8K
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

You might also read

Related Articles

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

Sort by
Same author

Adulthood depletion of Integrator extends lifespan and healthspan via defective pre-mRNA processing.

bioRxiv : the preprint server for biology·2026
Same author

Centromeres are hotspots of cytosine methylation epimutations in a filamentous fungus.

bioRxiv : the preprint server for biology·2026
Same author

EMBO Press co-evolves with molecular ecology and evolutionary biology.

The EMBO journal·2026
Same author

ATRX safeguards cellular identity during <i>C. elegans</i> development.

bioRxiv : the preprint server for biology·2026
Same author

Epimutations: raw material for evolution?

The EMBO journal·2026
Same author

UBA6 specificity for ubiquitin E2 conjugating enzymes reveals a priority mechanism of BIRC6.

Nature structural & molecular biology·2025

Related Experiment Video

Updated: Aug 22, 2025

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

DNA Methyltransferases and DNA Damage.

Peter Sarkies1

  • 1Department of Biochemistry, University of Oxford, London, UK. Peter.sarkies@bioch.ox.ac.uk.

Advances in Experimental Medicine and Biology
|November 9, 2022
PubMed
Summary

Cytosine DNA methyltransferases (DNMTs) impact DNA mutation rates by affecting DNA repair and directly causing DNA damage. This connection has implications for species evolution and human diseases like cancer.

Area of Science:

  • Genetics and Molecular Biology
  • Epigenetics
  • Evolutionary Biology

Background:

  • Cytosine DNA methyltransferases (DNMTs) are crucial enzymes involved in DNA methylation.
  • A known link exists between DNMTs and the accumulation of mutations in mammalian genomes.
  • Previous research highlighted DNMTs' indirect influence on mutation rates via DNA repair and mutation mechanisms.

Purpose of the Study:

  • To explore the multifaceted relationship between DNMTs and DNA damage.
  • To evaluate the consequences of DNMT-induced DNA damage on evolutionary processes.
  • To assess the role of DNMTs and DNA damage in human diseases, particularly cancer.

Main Methods:

  • Review of existing literature on DNMTs, DNA mutation, DNA repair, and DNA damage.
Keywords:
CancerDNA damageDNA methylationDNA repairEpigeneticsEvolutionMutation

More Related Videos

Continuous Fluorescence-Based Endonuclease-Coupled DNA Methylation Assay to Screen for DNA Methyltransferase Inhibitors
06:07

Continuous Fluorescence-Based Endonuclease-Coupled DNA Methylation Assay to Screen for DNA Methyltransferase Inhibitors

Published on: August 5, 2022

2.7K
Author Spotlight: Quantitative Detection of DNA Protein Crosslinks and Their Post-Translational Modifications
10:12

Author Spotlight: Quantitative Detection of DNA Protein Crosslinks and Their Post-Translational Modifications

Published on: April 21, 2023

2.9K

Related Experiment Videos

Last Updated: Aug 22, 2025

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
Continuous Fluorescence-Based Endonuclease-Coupled DNA Methylation Assay to Screen for DNA Methyltransferase Inhibitors
06:07

Continuous Fluorescence-Based Endonuclease-Coupled DNA Methylation Assay to Screen for DNA Methyltransferase Inhibitors

Published on: August 5, 2022

2.7K
Author Spotlight: Quantitative Detection of DNA Protein Crosslinks and Their Post-Translational Modifications
10:12

Author Spotlight: Quantitative Detection of DNA Protein Crosslinks and Their Post-Translational Modifications

Published on: April 21, 2023

2.9K
  • Analysis of studies investigating the direct and indirect effects of DNMTs on DNA integrity.
  • Examination of evolutionary and disease-related contexts where DNMTs play a role.
  • Main Results:

    • DNMTs influence mutation rates through both indirect effects on DNA repair and mutation pathways.
    • Emerging evidence suggests DNMTs can directly inflict damage on DNA.
    • These DNMT-mediated DNA alterations have significant implications for evolution and disease.

    Conclusions:

    • DNMTs are key players in maintaining genome stability, with a dual role in influencing mutation rates.
    • Understanding the direct DNA damaging potential of DNMTs is critical for comprehending their impact on evolution and disease.
    • Further research into DNMTs' role in DNA damage is warranted for insights into cancer and evolutionary trajectories.