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

10.4K
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...
10.4K
DNA Damage Can Stall the Cell Cycle02:36

DNA Damage Can Stall the Cell Cycle

3.4K
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...
3.4K
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
S-Cdk Initiates DNA Replication02:38

S-Cdk Initiates DNA Replication

5.9K
The cell cycle is a series of events leading to DNA duplication followed by the division of cell content to form two daughter cells. The cell cycle progresses in four stages—the cell increases in size (gap 1 or G1-phase), duplicates its DNA (synthesis or S-phase), prepares to divide (gap 2 or G2-phase), and divides (mitosis or M-phase).
Two states at the origin of replication
In eukaryotes, the initiation of replication occurs at many sites on the chromosomes, called the origins of...
5.9K
S-Cdk Initiates DNA Replication02:38

S-Cdk Initiates DNA Replication

3.5K
3.5K
The DNA Replication Fork01:02

The DNA Replication Fork

43.0K
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...
43.0K

You might also read

Related Articles

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

Sort by
Same author

The promise of adaptive health in the United Arab Emirates and beyond.

Nature genetics·2026
Same author

Non-Mendelian inheritance of DNA methylation patterns in mice.

Nature genetics·2026
Same author

DNA Methylation Stochasticity Is Linked to Transcriptional Variability and Convergent Epigenetic Disruption across Genetic Subtypes of Acute Myeloid Leukemia.

Cancer research·2026
Same author

Convergence of aging- and rejuvenation-related epigenetic alterations on PRC2 targets.

Molecular systems biology·2026
Same author

CRISPR screen of human pancreatic cancer xenografts identifies a KLF5 proliferation vulnerability through epigenetic modifiers NCAPD2 and MTHFD1.

Molecular cancer·2026
Same author

Spatially resolved molecular sex differences at single-cell resolution in the adult human ventromedial and arcuate hypothalamus.

Cell reports·2026

Related Experiment Video

Updated: Mar 29, 2026

Immunostaining for DNA Modifications: Computational Analysis of Confocal Images
09:42

Immunostaining for DNA Modifications: Computational Analysis of Confocal Images

Published on: September 7, 2017

10.4K

DNA methylation is stable during replication and cell cycle arrest.

Amy R Vandiver1, Adrian Idrizi1, Lindsay Rizzardi1

  • 1Center for Epigenetics, Johns Hopkins University School of Medicine.

Scientific Reports
|December 10, 2015
PubMed
Summary

Global DNA methylation levels remain stable during cell replication and arrest. This study found no evidence of large hypomethylated blocks in different cell cycle phases, challenging previous assumptions in cancer research.

More Related Videos

Examination of Proteins Bound to Nascent DNA in Mammalian Cells Using BrdU-ChIP-Slot-Western Technique
09:14

Examination of Proteins Bound to Nascent DNA in Mammalian Cells Using BrdU-ChIP-Slot-Western Technique

Published on: January 14, 2016

9.6K
Assessing Cell Cycle Progression of Neural Stem and Progenitor Cells in the Mouse Developing Brain after Genotoxic Stress
09:51

Assessing Cell Cycle Progression of Neural Stem and Progenitor Cells in the Mouse Developing Brain after Genotoxic Stress

Published on: May 7, 2014

15.9K

Related Experiment Videos

Last Updated: Mar 29, 2026

Immunostaining for DNA Modifications: Computational Analysis of Confocal Images
09:42

Immunostaining for DNA Modifications: Computational Analysis of Confocal Images

Published on: September 7, 2017

10.4K
Examination of Proteins Bound to Nascent DNA in Mammalian Cells Using BrdU-ChIP-Slot-Western Technique
09:14

Examination of Proteins Bound to Nascent DNA in Mammalian Cells Using BrdU-ChIP-Slot-Western Technique

Published on: January 14, 2016

9.6K
Assessing Cell Cycle Progression of Neural Stem and Progenitor Cells in the Mouse Developing Brain after Genotoxic Stress
09:51

Assessing Cell Cycle Progression of Neural Stem and Progenitor Cells in the Mouse Developing Brain after Genotoxic Stress

Published on: May 7, 2014

15.9K

Area of Science:

  • Epigenetics
  • Molecular Biology
  • Genomics

Background:

  • DNA methylation is a crucial epigenetic modification regulating gene expression during development.
  • Global DNA hypomethylation is a recognized hallmark of cancer and is also observed in EBV transformation and replicative senescence.
  • Previous studies linked large genomic blocks of hypomethylation to conditions altering the proportion of actively proliferating cells.

Purpose of the Study:

  • To investigate whether cell replication or cell-cycle arrest influences global DNA methylation levels.
  • To determine if cell cycle dynamics lead to the formation of large hypomethylated blocks, similar to those seen in cancer.

Main Methods:

  • Primary dermal fibroblasts were isolated into distinct cell cycle phases (G0, G1, G2) using fluorescence-activated cell sorting (FACS) based on DNA content and Ki67 staining.
  • Extended G0 arrest was induced via contact inhibition for one week.
  • Genome-wide DNA methylation analysis was performed on sorted cells using whole-genome bisulfite sequencing (WGBS).

Main Results:

  • Analysis of DNA methylation across different cell cycle phases (G0, G1, G2) revealed no significant global changes in methylation levels.
  • No large-scale hypomethylated blocks were identified in primary fibroblasts regardless of their cell cycle status or duration of arrest.
  • Global DNA methylation appears to be stable and not affected by replication or cell-cycle arrest in primary dermal fibroblasts.

Conclusions:

  • Cell cycle progression and arrest do not induce global DNA hypomethylation or the formation of large hypomethylated genomic blocks.
  • The stability of global DNA methylation levels suggests that other epigenetic or genetic factors are primarily responsible for hypomethylation observed in cancer and senescence.
  • Findings indicate that cell cycle phase is not a direct driver of the large-scale hypomethylation patterns seen in disease states.