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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).
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
Mutations in Microorganisms01:18

Mutations in Microorganisms

Mutations are heritable changes in an organism’s genome involving alterations in the base sequence of DNA or RNA. These changes can influence cellular processes and phenotypic traits, potentially transforming the unaltered wild type into a mutant form. Such changes, termed forward mutations, are pivotal in shaping the genetic diversity of organisms.RNA viruses exhibit the highest mutation rates due to the absence of robust proofreading mechanisms during genome replication. In contrast,...
In vitro Mutagenesis01:16

In vitro Mutagenesis

To learn more about the function of a gene, researchers can observe what happens when the gene is inactivated or “knocked out,” by creating genetically engineered knockout animals. Knockout mice have been particularly useful as models for human diseases such as cancer, Parkinson’s disease, and diabetes.
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...

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Updated: Jun 27, 2026

Gene-targeted Random Mutagenesis to Select Heterochromatin-destabilizing Proteasome Mutants in Fission Yeast
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Published on: May 15, 2018

Spontaneous mutagenesis is elevated in protease-defective cells.

Abu Amar M Al Mamun1, M Zafri Humayun

  • 1University of Medicine and Dentistry of New Jersey-New Jersey Medical School, Department of Microbiology and Molecular Genetics, International Center for Public Health, Newark, NJ 07101, USA.

Molecular Microbiology
|December 2, 2008
PubMed
Summary

The ClpXP protease prevents DNA mutations by degrading damaged proteins. Its absence leads to increased frameshift mutations, particularly those involving DNA polymerase IV (DinB).

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Identifying DNA Mutations in Purified Hematopoietic Stem/Progenitor Cells
11:06

Identifying DNA Mutations in Purified Hematopoietic Stem/Progenitor Cells

Published on: February 24, 2014

Area of Science:

  • Molecular Biology
  • Genetics
  • Microbiology

Background:

  • Proteolysis plays a crucial role in cellular maintenance, including genomic integrity.
  • The ClpXP protease is a major cytoplasmic protease involved in degrading various proteins.
  • Understanding ClpXP's role in mutagenesis is essential for comprehending DNA repair mechanisms.

Purpose of the Study:

  • To investigate the effect of ClpXP protease deficiency on spontaneous mutagenesis.
  • To identify the types of mutations and the molecular pathways involved in ClpXP-mediated mutagenesis.

Main Methods:

  • Assessing base substitution mutations using a rifampicin resistance assay.
  • Analyzing frameshift mutations via colony papillation and quantitative valine resistance assays.
  • Investigating the involvement of SOS response genes (lexA, dinB, umuC, umuD) and rpoS.

Main Results:

  • Loss of ClpXP protease moderately increased base substitution mutations.
  • A significant 50-fold increase in frameshift mutations was observed in ClpXP-deficient cells.
  • Elevated frameshift mutagenesis was dependent on the SOS gene dinB and abolished in SOS-uninducible cells.
  • Mutagenesis was not affected by loss of umuC/umuD or rpoS.

Conclusions:

  • ClpXP-mediated proteolysis is critical for preventing spontaneous frameshift mutagenesis.
  • Elevated DinB (DNA polymerase IV) expression and UmuD/UmuD' stabilization contribute to mutagenesis in ClpXP-deficient cells.
  • ClpXP protease activity is a key factor in maintaining genomic stability by limiting gratuitous mutagenesis.