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Processing DNA lesions during mitosis to prevent genomic instability

Anastasia Audrey1, Lauren de Haan1, Marcel A T M van Vugt1

  • 1Department of Medical Oncology, University Medical Center Groningen, Hanzeplein 1, 9713GZ Groningen, The Netherlands.

Biochemical Society Transactions
|August 30, 2022
PubMed

Insights

Cancer cells often carry DNA damage into mitosis. This review explores how cells process these mitotic DNA lesions, focusing on repair mechanisms and the impact on genome stability.

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Genetics

Background:

  • Failure to repair double-strand breaks (DSBs) causes genome instability, a cancer hallmark.
  • Canonical DSB repair pathways are inactive during mitosis.
  • Cancer cells frequently exhibit DNA lesions in mitosis, bypassing checkpoints.

Purpose of the Study:

  • To review how mitotic cells handle DNA lesions that evade checkpoint surveillance.
  • To outline mechanisms of the mitotic DNA damage response.
  • To discuss processing pathways for various mitotic DNA lesions.

Main Methods:

  • Literature review of DNA repair and cell cycle regulation.
  • Analysis of mechanisms for processing mitotic DNA lesions.
  • Focus on joint DNA molecules and DNA catenanes.

Main Results:

  • Mitotic cells employ specific pathways to process lesions like joint DNA molecules and catenanes.
  • Mechanisms regulating the mitotic DNA damage response are crucial.
  • Under-replication and recombination intermediates are key lesion types.

Conclusions:

  • Unresolved mitotic DNA lesions have significant consequences for cellular fate.
  • Mitotic processing of DNA damage is critical for maintaining genome stability.
  • Understanding these pathways is vital for cancer research.
Keywords:
DNA damage responsecell cyclegenome instabilitygenome integritymitosis

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