The transcription factor encoded by the Sox10 gene is important in neural crest development, melanocyte development and homeostasis, myelination and mammary epithelial cell development. These Sox10-iCreER^T2 mutant mice carry a transgene with tamoxifen-inducible optimized (improved) Cre recombinase under the control of the mouse Sox10 (SRY (sex determining region Y)-box 10) promoter. iCre is an "improved Cre", optimized with mammalian codon usage, removed putative cryptic splice sites, an altered stop codon, and reduced CpG content to limit the chances of epigenetic silencing in mammals. When crossed with a strain containing a loxP site flanked sequence of interest, the offspring are useful for generating tamoxifen-induced, iCre-mediated targeted deletions. Tamoxifen administration induces Cre recombination in oligodendrocyte lineage cells. When crossed to a ROSA-YFP reporter strain, the resulting double mutant mice, treated with tamoxifen, exhibited YFP expression in more than 90% of Sox10 expressing cells in the spinal cord, and 65% of Sox10 expressing cells in the cerebral cortex and corpus callosum one week after treatment. Homozygotes are viable and fertile. The Donating Investigator reports that there is no difference in phenotype between homozygotes and hemizygotes.

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 (17ß-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.