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Carcinogens induce reversion of the mouse pink-eyed unstable mutation

R H Schiestl1, J Aubrecht, F Khogali

  • 1Department of Molecular and Cellular Toxicology, Harvard School of Public Health, 665 Huntington Avenue, Boston, MA 02115, USA. schiestl@mbcrr.harvard.edu

Insights

Carcinogen exposure can induce genome rearrangements, specifically deletions, in mice with the pink-eyed unstable (pun) mutation. These DNA deletion assays show promise as sensitive indicators for carcinogen exposure.

Area of Science:

  • Genetics
  • Molecular Biology
  • Toxicology

Background:

  • Genome rearrangements like deletions are linked to cancer and inherited diseases.
  • The pink-eyed unstable (pun) mutation in mice involves a duplicated p gene fragment.
  • Spontaneous reversion in pun/pun mice occurs via deletion of this duplicated sequence.

Purpose of the Study:

  • To investigate the molecular mechanism of carcinogen-induced reversion events in the pun mouse model.
  • To determine if DNA deletion assays can serve as sensitive indicators for carcinogen exposure.

Main Methods:

  • Utilizing the pink-eyed unstable (pun) mouse model.
  • Inducing reversion events with various carcinogens (x-rays, EMS, MMS, ENU, B[a]P, TCE, benzene, sodium arsenate).
  • Employing cDNA analysis with reverse transcriptase-PCR to identify molecular changes.

Main Results:

  • Carcinogen exposure successfully induced reversion events in premelanocytes.
  • Identified induced reversion events as deletions at the molecular level.
  • Demonstrated that certain carcinogens (TCE, benzene, sodium arsenate) induce deletions detectable by this assay, despite failing other mutagenesis assays.

Conclusions:

  • Carcinogen-induced DNA deletions are a key mechanism in the reversion of the pun mutation.
  • DNA deletion assays represent a potentially sensitive method for detecting exposure to genotoxic carcinogens.
  • This mouse model provides insights into genome instability and carcinogenesis.

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