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Cell-Cycle Asynchrony Generates DNA Damage at Mitotic Entry in Polyploid Cells.
Maddalena Nano1, Simon Gemble1, Anthony Simon1
1Biology of Centrosomes and Genetic Instability Lab, Institut Curie, PSL Research University, CNRS UMR144, 12 rue Lhomond, 75005 Paris, France.
Current Biology : CB
|November 12, 2019
Summary
Polyploidy, or whole-genome duplication, can cause DNA damage in dividing cells. This damage arises when cells enter mitosis asynchronously, potentially driving cancer genome instability.
Area of Science:
- Cell Biology
- Genetics
- Cancer Research
Background:
- Polyploidy, the gain of complete chromosome sets, is linked to cancer genome evolution.
- Whole-genome duplications (WGDs) are frequent in human tumors, potentially accelerating karyotype abnormalities.
- The molecular links between WGD and genetic instability are not fully understood.
Purpose of the Study:
- To investigate the consequences of polyploidy in vivo.
- To elucidate the mechanisms by which polyploidy induces genetic instability.
- To determine if polyploidy causes DNA damage during cell division.
Main Methods:
- Induced polyploidization in Drosophila neural stem cells (NSCs) via repeated cytokinesis failure.
- Confirmed findings in mouse NSCs and human cancer cells after cytokinesis inhibition.
- Analyzed cell-cycle asynchrony and DNA damage in polyploid cells.
Main Results:
- Polyploidy induced DNA damage in a subset of nuclei within polyploid neuroblasts during mitosis.
- DNA damage occurred in nuclei not prepared for mitosis but forced into it.
- Polyploid cells exhibited cell-cycle asynchrony, and synchronization reduced DNA damage.
Conclusions:
- DNA damage at mitotic entry in polyploid cells can lead to structural abnormalities.
- This mechanism may contribute to the development of genetic instability in cancer.
- Findings in Drosophila were validated in mammalian and human cancer cells.
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