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Related Concept Videos

DNA Damage can Stall the Cell Cycle02:36

DNA Damage can Stall the Cell Cycle

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...
DNA Damage Can Stall the Cell Cycle02:36

DNA Damage Can Stall the Cell Cycle

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...
Overview of DNA Repair02:25

Overview of DNA Repair

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.
Chemically...
Overview of DNA Repair02:25

Overview of DNA Repair

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.
Chemically...
Nucleotide Excision Repair01:38

Nucleotide Excision Repair

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...
Nucleotide Excision Repair01:08

Nucleotide Excision Repair

Overview

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Related Experiment Video

Updated: Jun 26, 2026

Visualizing and Quantifying Endonuclease-Based Site-Specific DNA Damage
10:59

Visualizing and Quantifying Endonuclease-Based Site-Specific DNA Damage

Published on: August 21, 2021

DNA damage tolerance: when it's OK to make mistakes.

Debbie J Chang1, Karlene A Cimprich

  • 1Department of Chemical and Systems Biology, Stanford University School of Medicine, Clark Center, 318 Campus Drive, W350B, Stanford, California 94305-5441, USA.

Nature Chemical Biology
|January 17, 2009
PubMed
Summary

DNA damage tolerance mechanisms, including translesion synthesis and template switching, are regulated by PCNA ubiquitination at stalled replication forks to ensure genome stability and DNA replication completion.

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Visualizing and Quantifying Endonuclease-Based Site-Specific DNA Damage
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Laser Microirradiation to Study In Vivo Cellular Responses to Simple and Complex DNA Damage
10:44

Laser Microirradiation to Study In Vivo Cellular Responses to Simple and Complex DNA Damage

Published on: January 31, 2018

Area of Science:

  • Molecular Biology
  • Genetics
  • Cell Biology

Background:

  • Mutations can be beneficial or detrimental, leading to genetic diversity or diseases like cancer.
  • DNA damage, particularly during S phase, poses a significant threat to genome integrity.
  • Replication fork stalling due to DNA lesions necessitates bypass mechanisms to ensure replication completion.

Purpose of the Study:

  • To discuss the regulation of DNA damage tolerance mechanisms at stalled replication forks.
  • To elucidate the roles of translesion synthesis and template switching in bypassing DNA lesions.
  • To explore the involvement of PCNA ubiquitination in controlling these tolerance pathways.

Main Methods:

  • Focuses on the regulatory mechanisms of DNA damage tolerance.
  • Discusses the roles of translesion synthesis and template switching.
  • Highlights the importance of PCNA ubiquitination in controlling lesion bypass.

Main Results:

  • DNA damage tolerance mechanisms are crucial for bypassing DNA lesions during S phase.
  • PCNA ubiquitination is a key regulatory event at stalled replication forks.
  • Both error-prone and error-free lesion bypass pathways are controlled by this ubiquitination.

Conclusions:

  • PCNA ubiquitination governs the choice between different DNA damage tolerance pathways.
  • Understanding these mechanisms is vital for comprehending genome stability and disease prevention.
  • This regulation ensures the accurate replication of damaged DNA, preventing potentially lethal mutations.