Targeted oncogene activation by site-specific recombination in transgenic mice

Proc Natl Acad Sci U S A. 1992 Jul 15;89(14):6232-6. doi: 10.1073/pnas.89.14.6232.

Abstract

An efficient and accurate method for controlled in vivo transgene modulation by site-directed recombination is described. Seven transgenic mouse founder lines were produced carrying the murine lens-specific alpha A-crystallin promoter and the simian virus 40 large tumor-antigen gene sequence, separated by a 1.3-kilobase-pair Stop sequence that contains elements preventing expression of the large tumor-antigen gene and Cre recombinase recognition sites. Progeny from two of these lines were mated with transgenic mice expressing the Cre recombinase under control of either the murine alpha A-crystallin promoter or the human cytomegalovirus promoter. All double-transgenic offspring developed lens tumors. Subsequent analysis confirmed that tumor formation resulted from large tumor-antigen activation via site-specific, Cre-mediated deletion of Stop sequences.

MeSH terms

  • Animals
  • Antigens, Polyomavirus Transforming / genetics*
  • Base Sequence
  • Cataract / genetics
  • DNA Nucleotidyltransferases / genetics
  • Eye Neoplasms / genetics
  • Integrases*
  • Mice
  • Mice, Transgenic
  • Molecular Sequence Data
  • Oligodeoxyribonucleotides / chemistry
  • Oncogenes*
  • Recombination, Genetic
  • Regulatory Sequences, Nucleic Acid
  • Viral Proteins*

Substances

  • Antigens, Polyomavirus Transforming
  • Oligodeoxyribonucleotides
  • Viral Proteins
  • Cre recombinase
  • DNA Nucleotidyltransferases
  • Integrases