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SOS induction and mutagenesis by dnaQ missense alleles in wild type cells

Satyendra Gautam1, Raju Kalidindi, M Zafri Humayun

  • 1University of Medicine and Dentistry of New Jersey - New Jersey Medical School, Department of Microbiology and Molecular Genetics, 225 Warren Street, ICPH-E450V, Newark NJ 07101-1709, United States.

Mutation Research
|June 9, 2012
PubMed

Insights

Mistranslation causes DNA damage and replication errors, potentially due to mixed protein populations. Proofreading subunit mutations and streptomycin exposure induce cellular stress responses, supporting this hypothesis.

Area of Science:

  • Molecular Biology
  • Genetics
  • Microbiology

Background:

  • Mistranslation, or the production of incorrect proteins, is linked to DNA damage.
  • The DNA polymerase III proofreading subunit (DnaQ) is crucial for DNA replication fidelity.
  • Aminoglycoside antibiotics like streptomycin are known to induce mistranslation.

Purpose of the Study:

  • To investigate the consequences of mistranslation on DNA fidelity and cellular responses.
  • To determine if mutations in the DNA polymerase III proofreading subunit (dnaQ) lead to mutagenesis and SOS induction.
  • To examine the effect of streptomycin on cellular stress responses.

Main Methods:

  • Expressing missense alleles of the dnaQ gene in wild-type cells.
  • Monitoring for mutagenesis and SOS induction.
  • Exposing cells to sublethal concentrations of streptomycin.

Main Results:

  • Expression of dnaQ missense alleles induced both mutagenesis and SOS response.
  • Streptomycin exposure also led to SOS induction, consistent with promoting mistranslation.
  • These findings support the hypothesis that mixed populations of wild-type and mistranslated proteins cause DNA damage.

Conclusions:

  • Mistranslation contributes to elevated mutagenesis and replication stress.
  • The DNA polymerase III proofreading subunit plays a key role in preventing these errors.
  • Cellular responses like SOS induction are triggered by mistranslation-induced DNA damage.

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