These transgenic mice express a tamoxifen inducible Cre recombinase, ERT2/cre/ERT2, driven by the mouse Sox10 MCS4 enhancer/c-Fos minimal promoter.
ERT2/cre/ERT2 (also known as ERiCreER) has been shown to tightly regulate inducible Cre recombinase activity with no detectable recombination activity without 4-hydroxytamoxifen.
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 neural crest cells. Heterozygotes are viable and fertile. The Donating Investigator has not attempted to make the strain homozygous, but predicts homozygotes would be viable.
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 and ERT2/cre/ERT2 (also known as ERiCreER) 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.
