A CreER^T2 fusion protein, and an internal ribosome entry site (IRES)-β-galactosidase (lacZ) gene replace the ATG start codon of the prominin 1 (Prom1) gene, abolishing gene expression. PROM1 is a transmembrane glycoprotein expressed on the surface of stem cells. In this strain, endogenous Prom1 promoter/enhancer regions drive lacZ expression in embryonic central nervous system, kidney, intestine, and skeletal system. In adults, expression is seen in acinar and islet cells of the pancreas, goblet and columnar epithelial cells of the colon, photorepectoprs of the eye, renal tube cells, brain, lung, and both male and female reproductive systems. Cre-ER^T2 fusion gene activity is inducible and only observed following tamoxifen administration. When these Prom1^C-L mice are bred with mice containing loxP-flanked sequence, tamoxifen-inducible, Cre-mediated recombination will result in deletion of the floxed sequences in the Prom1-expressing cells of the offspring. For example when bred to Gt(ROSA)26Sor^tm1(EYFP)Cos/J mice (Stock No. 006148), tamoxifen induction results in cre expression in small intestinal crypt cells and the epithelial surface of the villi. Homozygotes are viable and fertile, but are blind due to retinal pigmentosa.

The Cre-ER^T2 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-ER^T2 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.