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Cdk1-dependent lamin aggregation underlies oxidative stress-induced nuclear shape abnormalities.

Ju-Hyun Ahn1, Min-Guk Cho2, Abdul Basit3

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Reactive oxygen species (ROS) disrupt nuclear morphology in mitotic cells by reducing Cdk1 activity, causing lamin aggregation and affecting nuclear envelope reassembly. This reveals a novel mechanism of ROS-induced nuclear damage during cell division.

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Area of Science:

  • Cell Biology
  • Cancer Research
  • Molecular Biology

Background:

  • Altered nuclear morphology is a hallmark of cancer and impacts tumor prognosis.
  • Reactive oxygen species (ROS) are known to induce nuclear changes, but the mechanisms are unclear, especially during nuclear assembly.
  • Mitotic cells, with their dynamic nuclear envelope, may be particularly vulnerable to ROS-induced nuclear deformation.

Purpose of the Study:

  • To investigate the mechanism by which ROS affect nuclear morphology during mitosis.
  • To explore the role of hydrogen peroxide (H2O2) in mitotic nuclear assembly and deformation.
  • To elucidate the relationship between ROS, Cdk1 activity, and lamin dynamics.

Main Methods:

  • Exposure of mitotic cells to hydrogen peroxide (H2O2).
  • Analysis of lamin aggregation and nuclear morphology.
  • In vitro kinase assays to assess Cdk1 activity and lamin phosphorylation.
  • Investigating the effect of Cdk1 activity restoration on lamin aggregation.

Main Results:

  • H2O2 exposure in mitotic cells led to persistent lamin aggregates and aberrant nuclear morphology.
  • H2O2 dampened Cdk1 activity, reducing lamin phosphorylation and causing aggregation.
  • Restoring Cdk1 activity rescued lamin phosphorylation and mitigated aggregation.
  • Lamin aggregation during mitotic entry correlated with premature reassembly, disrupting nuclear envelope formation.

Conclusions:

  • ROS-mediated perturbation of Cdk1 activity during early mitosis triggers lamin aggregation.
  • This aggregation disrupts lamin reassembly and nuclear envelope formation, leading to altered nuclear morphology.
  • The study reveals a novel mechanism of ROS-induced nuclear architecture disruption via Cdk1 modulation during mitosis.