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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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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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Meiosis II entails cell division and segregation of the sister chromatids, resulting in the production of four unique haploid gametes. The steps for meiosis II are similar to mitosis, except that meiosis II occurs in haploid cells, whereas mitosis occurs in diploid cells.
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Meiosis II01:57

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Meiosis II is the second and final stage of meiosis. It relies on the haploid cells produced during meiosis I, each of which contain only 23 chromosomes—one from each homologous initial pair. Importantly, each chromosome in these cells is composed of two joined copies, and when these cells enter meiosis II, the goal is to separate such sister chromatids using the same microtubule-based network employed in other division processes. The result of meiosis II is two haploid cells, each...
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Epigenetic Regulation01:37

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Epigenetic changes alter the physical structure of the DNA without changing the genetic sequence and often regulate whether genes are turned on or off. This regulation ensures that each cell produces only proteins necessary for its function. For example, proteins that promote bone growth are not produced in muscle cells. Epigenetic mechanisms play an essential role in healthy development. Conversely, precisely regulated epigenetic mechanisms are disrupted in diseases like cancer.
X-chromosome...
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Epigenetic mechanisms play an essential role in healthy development. Conversely, precisely regulated epigenetic mechanisms are disrupted in diseases like cancer.
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Visualizing and Quantifying Endonuclease-Based Site-Specific DNA Damage
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SOX2 phosphorylation during mitosis limits genomic damage.

Charles A C Williams1,2, Dounia Djeghloul3, Nicolas Veland3

  • 1Centre for Regenerative Medicine, Institute for Regeneration and Repair, Cancer Research UK Scotland Centre, University of Edinburgh, Edinburgh EH16 4UU, United Kingdom.

Genes & Development
|November 10, 2025
PubMed
Summary
This summary is machine-generated.

SOX2 phosphorylation regulates its binding to DNA during cell division. Uncontrolled SOX2 activity in cancer promotes stemness and chromosomal damage, indicating dual oncogenic roles.

Keywords:
DNA damageSOX2heterochromatinmitosismitotic bookmarkingneural stem cellphosphorylationtranscription

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Area of Science:

  • Molecular Biology
  • Cancer Research
  • Stem Cell Biology

Background:

  • Pioneer transcription factors (TFs) like SOX2 control stem cell identity.
  • SOX2 is crucial for neural stem cell (NSC) self-renewal and is often overexpressed in glioblastoma stem cells (GSCs).
  • Dysregulated SOX2 contributes to cancer development and progression.

Purpose of the Study:

  • To investigate the role of SOX2 phosphorylation in regulating its activity during NSC division.
  • To understand the consequences of excessive SOX2 pioneer activity on mitotic processes.
  • To elucidate the dual oncogenic functions of elevated SOX2 in cancer.

Main Methods:

  • Studied SOX2 phosphorylation during neural stem cell division.
  • Assessed the impact of SOX2 on chromatin binding and mitotic progression.
  • Investigated the relationship between SOX2 levels, mitotic damage, and chromosomal integrity.

Main Results:

  • SOX2 phosphorylation acts as a critical regulatory switch during mitosis, preventing widespread genomic binding.
  • Excessive SOX2 activity in mitosis leads to uncontrolled chromatin opening.
  • This unconstrained activity results in prolonged mitotic duration and increased chromosomal damage.

Conclusions:

  • SOX2 phosphorylation is essential for maintaining genomic stability during cell division.
  • Elevated SOX2 in cancers may promote stemness through transcriptional roles and induce genomic instability via unconstrained pioneer activity.
  • This dual mechanism highlights SOX2 as a significant driver of cancer progression and oncogenesis.