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Related Concept Videos

Nucleotide Excision Repair01:08

Nucleotide Excision Repair

Overview
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 Repair01:08

Nucleotide Excision Repair

Overview
Translesion DNA Polymerases02:10

Translesion DNA Polymerases

Translesion (TLS) polymerases rescue stalled DNA polymerases at sites of damaged bases by replacing the replicative polymerase and installing a nucleotide across the damaged site. Doing so, TLS allows additional time for the cell to repair the damage before resuming regular DNA replication.
TLS polymerases are found in all three domains of life - archaea, bacteria, and eukaryotes. Of the different classes of TLS polymerases, members of the Y family are fitted with specialized structures that...
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...
Spontaneous and Induced Mutations01:30

Spontaneous and Induced Mutations

Spontaneous mutations arise infrequently during DNA replication due to errors in the process. A key factor behind these errors is tautomeric shifts in nitrogenous bases, where bases transition from keto to enol forms or amino to imino forms. This shift can alter base-pairing rules, leading to mutations. Additionally, reactive oxygen species (ROS) arising from aerobic metabolism can damage DNA, resulting in depurination (loss of a purine base) or depyrimidination (loss of a pyrimidine base).

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Related Experiment Video

Updated: Jul 11, 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-induced mutation: tolerance via translesion synthesis.

B A Kunz1, A F Straffon, E J Vonarx

  • 1School of Biological and Chemical Sciences, Deakin University, Victoria 3217, Geelong, Australia. bkunz@deakin.edu.au

Mutation Research
|August 1, 2000
PubMed
Summary

Translesion synthesis (TLS) tolerates DNA damage in yeast and humans, primarily causing mutations rather than through error-prone repair. This process, involving specific DNA polymerases, impacts cancer risk, with error-free TLS potentially reducing skin cancer risk.

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Area of Science:

  • Molecular Biology
  • Genetics
  • Cancer Research

Background:

  • Translesion synthesis (TLS) is crucial for mutagenesis induced by DNA damage in Saccharomyces cerevisiae.
  • TLS acts as a DNA damage tolerance mechanism rather than an error-prone repair pathway.
  • Key proteins involved in yeast TLS are encoded by the RAD6 epistasis group, including specific DNA polymerases.

Purpose of the Study:

  • To review and link evidence of translesion synthesis in yeast to findings in mammalian cells.
  • To explore the role of nonreplicative DNA polymerases in DNA damage tolerance.
  • To connect TLS mechanisms to cancer risk in humans.

Main Methods:

  • Review of existing literature on translesion synthesis in yeast and mammalian cells.
  • Comparison of homologous proteins and pathways between yeast and mammals.
  • Analysis of the link between error-free and error-prone TLS and cancer risk.

Main Results:

  • TLS is essential for most damage-induced mutations in yeast, arising from DNA lesion tolerance.
  • Homologues of yeast RAD6 group proteins, including DNA polymerases, are found in mammalian cells.
  • Error-free TLS in humans is associated with reduced UV-induced skin cancer risk, while error-prone TLS may increase it.

Conclusions:

  • Translesion synthesis is a conserved mechanism for DNA damage tolerance across yeast and mammals.
  • The balance between error-free and error-prone TLS plays a significant role in modulating cancer risk.
  • Understanding TLS pathways offers insights into cancer prevention and treatment strategies.