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Related Concept Videos

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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Quantification of three DNA Lesions by Mass Spectrometry and Assessment of Their Levels in Tissues of Mice Exposed to Ambient Fine Particulate Matter
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Increased replication-associated single-stranded DNA promotes formaldehyde-induced mutagenesis.

Thomas Blouin1, Charlotte McGuinness1, Kierra Marshall1

  • 1Department of Biochemistry and Molecular Biology, Medical University of South Carolina, Charleston, SC, USA.

Biorxiv : the Preprint Server for Biology
|May 7, 2026
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Summary

Formaldehyde (FA) exposure causes DNA damage and mutations. Replication defects, particularly those creating single-stranded DNA (ssDNA), significantly elevate FA-induced mutagenesis by impacting DNA repair pathways.

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Published on: September 23, 2011

Area of Science:

  • Molecular Biology
  • Genetics
  • Toxicology

Background:

  • Formaldehyde (FA) is a ubiquitous environmental toxin and endogenous metabolite.
  • FA is known to induce DNA damage, mutagenesis, and carcinogenesis, often creating a specific mutation signature (SBS40).
  • Understanding the mechanisms underlying FA-induced mutagenesis is crucial for assessing its health risks.

Purpose of the Study:

  • To investigate the role of replication stress and single-stranded DNA (ssDNA) in formaldehyde-induced mutagenesis.
  • To identify specific DNA repair and replication pathways involved in processing FA-induced DNA damage.
  • To elucidate how cellular responses to FA impact mutagenesis outcomes.

Main Methods:

  • Utilized yeast models with genetic modifications affecting replicative polymerases and DNA repair pathways.
  • Assessed ssDNA accumulation and FA mutagenesis levels in response to genetic perturbations.
  • Investigated the roles of Mrc1 (CLASPIN), DNA-protein crosslink repair, Pol ζ, and template switching in FA mutagenesis.

Main Results:

  • Downregulation of major replicative polymerases leads to increased ssDNA and elevated FA mutagenesis.
  • Loss of Mrc1 (CLASPIN) causes significant ssDNA accumulation and FA mutagenesis, independent of its checkpoint function.
  • Impaired DNA-protein crosslink repair increases FA sensitivity but not mutagenesis.
  • FA-induced mutagenesis relies on Pol ζ-mediated translesion synthesis, while template switching is not essential for error-free bypass.

Conclusions:

  • Replication-associated ssDNA is a primary substrate for formaldehyde-induced DNA damage.
  • Specific pathways, including Pol ζ-dependent translesion synthesis, are critical in determining FA mutagenesis outcomes.
  • Cellular responses during replication stress dictate the mutagenic potential of formaldehyde exposure.