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Temporally controlled somatic mutagenesis in smooth muscle.

Ligand-dependent site-specific recombinases are powerful tools to engineer the mouse genome in specific somatic cell types at selected times during pre- and postnatal development. Current efforts are primarily directed towards increasing the efficiency of this recombination system in mice. We have generated transgenic mouse lines expressing a tamoxifen-activated Cre recombinase, CreER(T2), under the control of the smooth muscle-specific SM22 promoter. Both a randomly integrated transgene [SM-CreER(T2)(tg)] and a transgene that has been "knocked in" into the endogenous SM22 locus [SM-CreER(T2)(ki)] were expressed in smooth muscle-containing tissues. The level of CreER(T2) expression and tamoxifen-induced recombination was lower in SM-CreER(T2)(tg) mice compared with SM-CreER(T2)(ki) mice. Whereas no recombinase activity could be detected in vehicle-treated SM-CreER(T2)(ki) mice, administration of tamoxifen induced the excision of a loxP-flanked reporter transgene in up to 100% of smooth muscle cells. The recombined genome persisted for at least four months after tamoxifen treatment. SM-CreER(T2)(ki) transgenic mice should be useful to study the effects of various somatic mutations in smooth muscle.

Pubmed ID: 11020712


  • Kühbandner S
  • Brummer S
  • Metzger D
  • Chambon P
  • Hofmann F
  • Feil R


Genesis (New York, N.Y. : 2000)

Publication Data

September 15, 2000

Associated Grants


Mesh Terms

  • Animals
  • Gene Expression Regulation
  • Gene Targeting
  • Injections, Intraperitoneal
  • Integrases
  • Mice
  • Mice, Inbred C57BL
  • Mice, Transgenic
  • Microfilament Proteins
  • Muscle Proteins
  • Muscle, Smooth
  • Mutagenesis, Insertional
  • Organ Specificity
  • Promoter Regions, Genetic
  • RNA, Messenger
  • Receptors, Estrogen
  • Recombination, Genetic
  • Tamoxifen
  • Transgenes
  • Viral Proteins