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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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Synthesis of new DNA molecules is carried out by the enzyme DNA polymerase, which adds nucleotides on the daughter strand complementary to the template DNA strand. DNA polymerase has a higher affinity to add the correct base and ensures fidelity during DNA replication. Furthermore,  it exhibits proofreading activity during replication, using an exonuclease domain that cuts off incorrect nucleotides from the nascent DNA strand.
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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.
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Related Experiment Video

Updated: Dec 14, 2025

Assessing Teratogenic Changes in a Zebrafish Model of Fetal Alcohol Exposure
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Ethanol exposure increases mutation rate through error-prone polymerases.

Karin Voordeckers1,2, Camilla Colding3, Lavinia Grasso4

  • 1Laboratory of Systems Biology, VIB-KU Leuven Center for Microbiology, Leuven, Belgium.

Nature Communications
|July 23, 2020
PubMed
Summary
This summary is machine-generated.

Ethanol exposure causes DNA replication stress and mutations by recruiting error-prone polymerases to stalled replication forks. Preventing this recruitment reduces ethanol

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Area of Science:

  • Molecular Biology
  • Genetics
  • Biochemistry

Background:

  • Ethanol is a common environmental toxin affecting all organisms.
  • Understanding ethanol's genotoxic mechanisms is crucial for public health.

Purpose of the Study:

  • To investigate the molecular mechanisms by which ethanol induces DNA mutations.
  • To explore the role of DNA replication stress and polymerase recruitment in ethanol mutagenesis.

Main Methods:

  • Utilized the model eukaryote Saccharomyces cerevisiae.
  • Analyzed DNA replication dynamics, protein localization (Mrc1), and DNA polymerase recruitment.
  • Employed mutagenesis of PCNA/Pol30 and deletion of error-prone polymerases.

Main Results:

  • Sublethal ethanol concentrations induce DNA replication stress and increase mutation rates.
  • Ethanol alters Mrc1 localization and recruits error-prone DNA polymerases to replication forks.
  • Inhibiting polymerase recruitment prevents ethanol-induced mutagenesis.

Conclusions:

  • Ethanol's mutagenic effects stem from a mechanism involving replication fork dysfunction and error-prone polymerase recruitment.
  • Findings offer insights into ethanol-induced DNA damage and potential links to carcinogenesis.