Fiche publication
Date publication
octobre 1996
Journal
Proceedings of the National Academy of Sciences of the United States of America
Auteurs
Membres identifiés du Cancéropôle Est :
Pr CHAMBON Pierre
,
Dr METZGER Daniel
Tous les auteurs :
Feil R, Brocard J, Mascrez B, LeMeur M, Metzger D, Chambon P
Lien Pubmed
Résumé
Current mouse gene targeting technology is unable to introduce somatic mutations at a chosen time and/or in a given tissue. We report here that conditional site-specific recombination can be achieved in mice using a new version of the Cre/lox system. The Cre recombinase has been fused to a mutated ligand-binding domain of the human estrogen receptor (ER) resulting in a tamoxifen-dependent Cre recombinase, Cre-ERT, which is activated by tamoxifen, but not by estradiol. Transgenic mice were generated expressing Cre-ERT under the control of a cytomegalovirus promoter. We show that excision of a chromosomally integrated gene flanked by loxP sites can be induced by administration of tamoxifen to these transgenic mice, whereas no excision could be detected in untreated animals. This conditional site-specific recombination system should allow the analysis of knockout phenotypes that cannot be addressed by conventional gene targeting.
Mots clés
Animals, Gene Expression Regulation, Genetic Engineering, methods, Integrases, chemistry, Ligands, Mice, Mice, Transgenic, Receptors, Estrogen, chemistry, Recombinant Fusion Proteins, metabolism, Recombination, Genetic, Sequence Deletion, Tamoxifen, pharmacology, Transgenes, genetics, Viral Proteins
Référence
Proc. Natl. Acad. Sci. U.S.A.. 1996 Oct;93(20):10887-90
