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Related Concept Videos

DNA Damage can Stall the Cell Cycle02:37

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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 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.
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The basic reaction of homologous recombination (HR) involves two chromatids that contain DNA sequences sharing a significant stretch of identity. One of these sequences uses a strand from another as a template to synthesize DNA in an enzyme-catalyzed reaction. The final product is a novel amalgamation of the two substrates. To ensure an accurate recombination of sequences, HR is restricted to the S and G2 phases of the cell cycle. At these stages, the DNA has been replicated already and the...
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The double-stranded structure of DNA has two major advantages. First, it serves as a safe repository of genetic information where one strand serves as the back-up in case the other strand is damaged. Second, the double-helical structure can be wrapped around proteins called histones to form nucleosomes, which can then be tightly wound to form chromosomes. This way, DNA chains up to 2 inches long can be contained within microscopic structures in a cell. A double-stranded break not only damages...
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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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Visualizing and Quantifying Endonuclease-Based Site-Specific DNA Damage
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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
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Summary
This summary is machine-generated.

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.

Keywords:
DNA damage responsecell cyclegenome instabilitygenome integritymitosis

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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.