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Related Concept Videos

DNA Damage can Stall the Cell Cycle02:36

DNA Damage can Stall the Cell Cycle

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

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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...
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Mitogens and the Cell Cycle02:38

Mitogens and the Cell Cycle

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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...
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Overview of DNA Repair02:25

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

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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.
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Nucleotide Excision Repair

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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...
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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

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

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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.