Jove
Visualize
Contact Us

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
Mitogens and the Cell Cycle02:38

Mitogens and the Cell Cycle

8.4K
Mitogens and their receptors play a crucial role in controlling the progression of the cell cycle. However, the loss of mitogenic control over cell division leads to tumor formation. Therefore, mitogens and mitogen receptors play an important role in cancer research. For instance, the epidermal growth factor (EGF) - a type of mitogen and its transmembrane receptor (EGFR), decides the fate of the cell's proliferation. When EGF binds to EGFR, a member of the ErbB family of tyrosine kinase...
8.4K
Overview of DNA Repair02:25

Overview of DNA Repair

35.5K
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...
35.5K
Role Of Notch Signalling In Intestinal Stem Cell Renewal01:12

Role Of Notch Signalling In Intestinal Stem Cell Renewal

2.6K
Notch signaling was first discovered in Drosophila melanogaster, where it is involved in cell lineage differentiation. Notch signaling regulates the maintenance and differentiation of intestinal stem cells or ISCs by controlling the expression of atonal homolog 1 or Atoh1. Atoh1 directs cells to differentiate into secretory cells.
Direct cell-to-cell contact is needed for the activation of Notch signaling. The signal is initiated when a notch ligand binds to a receptor on an adjacent cell, also...
2.6K
Nucleotide Excision Repair01:38

Nucleotide Excision Repair

5.8K
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...
5.8K

You might also read

Related Articles

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

Sort by
Same author

<i>Tet</i> Trim-Away: A conditional rapid protein degradation system for <i>Tetrahymena thermophila</i>.

bioRxiv : the preprint server for biology·2026
Same author

Centrosome depletion rewires mitosis to impose dependence on the AURKA-TPX2 axis.

bioRxiv : the preprint server for biology·2026
Same author

The cell cycle variant in multiciliated cells incorporates 2 centriole biogenesis cycles.

bioRxiv : the preprint server for biology·2026
Same author

Centriolar satellites regulate <i>CEP350</i> mRNA localization and centrosome amplification.

bioRxiv : the preprint server for biology·2026
Same author

Big1 is a cell-cycle regulator linking cell size to basal body number in Tetrahymena thermophila.

Current biology : CB·2026
Same author

Lamin B receptor upregulation in metastatic melanoma causes nuclear envelope fragility in confined migration during cancer invasion.

Proceedings of the National Academy of Sciences of the United States of America·2026
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 Experiment Video

Updated: Apr 9, 2026

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

4.2K

The DNA damage response pathway is required for multiciliated cell differentiation.

Cayla E Jewett1, Andrew J Holland2, Chad G Pearson3

  • 1Department of Molecular Biology and Genetics, Johns Hopkins School of Medicine, North Wolfe Street, Baltimore, MD 21205, USA; Department of Cell and Developmental Biology, University of Colorado Anschutz Medical Campus, East 17(th) Avenue, Aurora, CO 80045, USA.

Current Biology : CB
|April 7, 2026
PubMed
Summary
This summary is machine-generated.

Multiciliated cells (MCCs) create hundreds of centrioles post-mitosis by accumulating DNA damage. DNA damage response kinases are essential for this process, revealing a novel cell cycle adaptation.

Keywords:
ATMDNA damageDNA-PKH2AXR-loopcell cyclecentriole amplificationcilia

More Related Videos

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

9.8K
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

14.7K

Related Experiment Videos

Last Updated: Apr 9, 2026

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

4.2K
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

9.8K
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

14.7K

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Developmental Biology

Background:

  • Multiciliated cells (MCCs) require hundreds of centrioles for motile cilia formation.
  • Centriole duplication is typically restricted to the S and G2 phases of the cell cycle.
  • The mechanism by which MCCs duplicate centrioles in a post-mitotic state remains unclear.

Purpose of the Study:

  • To investigate the role of DNA damage in centriole amplification during MCC differentiation.
  • To understand how MCCs bypass cell cycle constraints for centriole duplication.

Main Methods:

  • Analysis of DNA double-strand breaks during MCC differentiation.
  • Assessment of DNA damage response (DDR) kinase involvement in centriole and cilia biogenesis.
  • Investigation of RNA-DNA hybrids (R-loops) at sites of DNA damage.

Main Results:

  • Differentiating MCCs accumulate significant double-strand DNA breaks during centriole amplification.
  • DNA damage levels correlate with the number of centrioles produced.
  • DDR kinases are crucial for supporting centriole biogenesis and ciliogenesis.
  • Transcription-driven R-loops colocalize with DNA damage sites.

Conclusions:

  • Physiological DNA damage and DDR signaling are harnessed during MCC differentiation.
  • This process allows MCCs to overcome canonical cell cycle restrictions for centriole amplification.
  • A developmental program involving transcription-coupled DNA damage rewires the cell cycle for specialized cell formation.