These vil-Cre-ERT2 transgenic mice express a tamoxifen inducible Cre recombinase driven by the 9-kb mouse Vil1, villin 1, promoter. When crossed with a strain containing a loxP site flanked sequence of interest, the offspring are useful for generating tamoxifen-induced, Cre-mediated targeted deletions. Tamoxifen administration induces Cre recombination in the intestinal epithelia of the duodenum, jejunum, ileum, and proximal and distal colon. No recombination is detected in brain, lung or heart. Inducible Cre recombinase activity is detected in the visceral endoderm of E9 embryos and the intestinal epithelium in E12.5 embryos. Southern blot analysis of founder line 23 (Fo23) revealed a single copy insertion of the transgene. The Donating Investigator has not attempted to make this strain homozygous. Hemizygotes are viable and fertile. Homozygous viability/fertility has not been tested (January 2019).
The Cre-ERT2 fusion protein consists of Cre recombinase fused to a triple mutant form of the human estrogen receptor which does not bind its natural ligand (17β-estradiol) at physiological concentrations but will bind the synthetic estrogen receptor ligands 4-hydroxytamoxifen (OHT or tamoxifen) and, with lesser sensitivity, ICI 182780. Restricted to the cytoplasm, Cre-ERT2 can only gain access to the nuclear compartment after exposure to tamoxifen. To counteract the mixed estrogen agonist effects of tamoxifen injections, which can result in late fetal abortions in pregnant mice, progesterone may be coadministered.
