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Related Concept Videos

Mismatch Repair01:20

Mismatch Repair

Organisms are capable of detecting and fixing nucleotide mismatches that occur during DNA replication. This sophisticated process requires identifying the new strand and replacing the erroneous bases with correct nucleotides. Mismatch repair is coordinated by many proteins in both prokaryotes and eukaryotes.
The Mutator Protein Family Plays a Key Role in DNA Mismatch Repair
The human genome has more than 3 billion base pairs of DNA per cell. Prior to cell division, that vast amount of genetic...
Mismatch Repair01:36

Mismatch Repair

Overview
Mismatch Repair01:36

Mismatch Repair

Overview
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).
Mutations01:39

Mutations

Overview
Mutations01:35

Mutations

Mutations are changes in the sequence of DNA. These changes can occur spontaneously or they can be induced by exposure to environmental factors. Mutations can be characterized in a number of different ways: whether and how they alter the amino acid sequence of the protein, whether they occur over a small or large area of DNA, and whether they occur in somatic cells or germline cells.
Chromosomal Alterations Are Large-Scale Mutations
While point mutations are changes in a single nucleotide in...

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Related Experiment Video

Updated: Jun 3, 2026

Assessing Somatic Hypermutation in Ramos B Cells after Overexpression or Knockdown of Specific Genes
08:12

Assessing Somatic Hypermutation in Ramos B Cells after Overexpression or Knockdown of Specific Genes

Published on: November 1, 2011

Damage-induced localized hypermutability.

Lauranell H Burch1, Yong Yang, Joan F Sterling

  • 1National Institute of Environmental Health Sciences, Research Triangle Park, NC USA.

Cell Cycle (Georgetown, Tex.)
|March 17, 2011
PubMed
Summary

Genome instability near DNA breaks allows cells to tolerate damaged DNA. Restoration generates mutations, creating mutation clusters important for evolution and disease.

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Related Experiment Videos

Last Updated: Jun 3, 2026

Assessing Somatic Hypermutation in Ramos B Cells after Overexpression or Knockdown of Specific Genes
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Gene-targeted Random Mutagenesis to Select Heterochromatin-destabilizing Proteasome Mutants in Fission Yeast
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Gene-targeted Random Mutagenesis to Select Heterochromatin-destabilizing Proteasome Mutants in Fission Yeast

Published on: May 15, 2018

Area of Science:

  • Genetics
  • Molecular Biology
  • Evolutionary Biology

Background:

  • Genome instability is a constant threat, causing cancer and disease, but also driving evolution.
  • Instability near DNA breaks, such as uncapped telomeres and double-strand breaks, is a critical area of study.

Purpose of the Study:

  • To investigate genome instability at DNA ends in budding yeast.
  • To understand how cells tolerate and repair damaged DNA in these regions.

Main Methods:

  • Utilizing budding yeast as a model organism.
  • Employing genome-wide sequencing to analyze mutation patterns.
  • Investigating tolerance of UV-damaged DNA in subtelomeric regions.

Main Results:

  • Budding yeast tolerates extensive single-strand DNA (up to 20 kilobases) with UV damage near telomeres.
  • DNA repair processes, specifically error-prone translesion synthesis, introduce multiple mutations during double-strand break restoration.
  • Genome-wide analysis revealed localized hypermutability, resulting in mutation clusters in UV-irradiated cells.

Conclusions:

  • Cells can tolerate significant DNA damage and instability at their ends.
  • Damage-induced mutations generated by translesion synthesis contribute to genome plasticity.
  • This novel form of genome instability may influence evolutionary adaptation and disease development.