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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).
Mutagenicity and Carcinogenicity01:25

Mutagenicity and Carcinogenicity

Mutagenicity and carcinogenicity refer to the ability of drugs to cause genetic defects and induce cancer, respectively. The International Agency for Research on Cancer (IARC) classifies agents into four groups based on their carcinogenic potential. Group 1 agents are known human carcinogens; group 2A agents are probably carcinogenic to humans; group 3 agents lack data to support their role in carcinogenesis; and group 4 includes agents for which data support that they are not likely to be...
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.
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...
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...

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Updated: May 9, 2026

The Lambda Select cII Mutation Detection System
07:08

The Lambda Select cII Mutation Detection System

Published on: April 26, 2018

Sequence context modulation of polycyclic aromatic hydrocarbon-induced mutagenesis.

Parvathi Chary1, Michael P Stone, R Stephen Lloyd

  • 1Center for Research on Occupational and Environmental Toxicology, Oregon Health and Science University, Portland, Oregon.

Environmental and Molecular Mutagenesis
|August 6, 2013
PubMed
Summary

Benzo[a]pyrene-7,8-dihydrodiol-9,10-epoxide (BPDE) DNA adducts at N-ras codon 61 position 3 cause diverse mutations, including A to C and A to T transversions. BPDE adducts also block DNA synthesis, with stereochemistry influencing the mutation spectrum and replication termination.

Keywords:
BPDEDNA polymerasesmutagenesis

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Transgenic Rodent Assay for Quantifying Male Germ Cell Mutant Frequency
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Area of Science:

  • Chemical Biology
  • Molecular Biology
  • Genetics

Background:

  • DNA adducts, such as those formed by benzo[a]pyrene-7,8-dihydrodiol-9,10-epoxide (BPDE), are linked to mutagenesis and cellular transformation.
  • Previous studies showed BPDE adducts at N-ras codon 61 position 2 exclusively cause A to G transitions.

Purpose of the Study:

  • To investigate the mutagenic potential and replication consequences of BPDE adducts at N-ras codon 61 position 3.
  • To determine if adduct stereochemistry influences mutation spectra and DNA synthesis termination.

Main Methods:

  • Replication of DNA containing C10 S-BPDE and C10 R-BPDE lesions at N-ras codon 61 position 3 in Escherichia coli.
  • Analysis of mutation spectra using various DNA polymerases (Sequenase 2.0, E. coli Klenow fragment, pol II).
  • Primer extension assays to assess DNA synthesis termination by the adducts.

Main Results:

  • Replication of BPDE adducts at position 3 yielded a broad mutation spectrum, including A to G transitions, A to C transversions (C10 S-BPDE), and A to T transversions (C10 R-BPDE).
  • DNA polymerases exhibited high fidelity synthesis with a consistent preference opposite the lesions, irrespective of sequence context.
  • BPDE adducts at position 3 caused significant DNA synthesis termination, with C10 S-BPDE being more blocking than C10 R-BPDE, and termination was more pronounced at position 3 than position 2.

Conclusions:

  • The position and stereochemistry of BPDE adducts significantly influence the resulting mutation spectrum and the fidelity of DNA replication.
  • BPDE adducts act as significant blocks to DNA synthesis, with implications for understanding genotoxicity and cellular response to carcinogens.