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Updated: Aug 7, 2026

Visualizing and Quantifying Endonuclease-Based Site-Specific DNA Damage
Published on: August 21, 2021
Cellular responses to DNA damage: one signal, multiple choices
1Molecular, Cellular and Developmental Biology, University of Colorado, Boulder, Colorado 80309-0347, USA. Tin.su@colorado.edu
Abstract:
DNA double-strand breaks (DSBs) produce a number of cellular responses, some mutually exclusive. Depending on where on the chromosome it occurs, a DSB may become preserved inside a telomere or eliminated by repair. A cell may arrest division via checkpoint activation to fix DSBs or commit suicide by apoptosis. What determines the outcome: to bury, fix, or succumb to DNA DSBs? With this question in mind, we review recent data on cellular responses to DSBs.
Insights
Cellular responses to DNA double-strand breaks (DSBs) vary, leading to repair, telomere preservation, or apoptosis. This review explores factors determining these outcomes for DNA repair.
Area of Science:
- Molecular Biology
- Cellular Biology
- Genetics
Background:
- DNA double-strand breaks (DSBs) are critical DNA lesions.
- Cellular responses to DSBs can be mutually exclusive.
- Outcomes include repair, telomere preservation, or apoptosis.
Purpose of the Study:
- To review recent data on cellular responses to DSBs.
- To understand the factors determining DSB fate.
- To explore mechanisms of DNA repair, telomere maintenance, and apoptosis.
Main Methods:
- Literature review of recent data on DSB cellular responses.
- Analysis of factors influencing DSB outcomes.
- Synthesis of information on cell cycle arrest, DNA repair pathways, and programmed cell death.
Main Results:
- DSB location influences whether it is repaired or preserved in telomeres.
- Checkpoint activation leads to cell division arrest for DSB repair.
- Alternatively, cells may undergo apoptosis in response to DSBs.
Conclusions:
- The cell's decision to repair, preserve, or undergo apoptosis depends on DSB characteristics and cellular context.
- Understanding these outcomes is crucial for comprehending genome stability.
- Further research is needed to fully elucidate the regulatory mechanisms governing DSB fate.
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