These Tyr::Cre-ERT2 transgenic mice carry a transgene with tamoxifen-inducible Cre recombinase under the control of the mouse tyrosinase (Tyr) gene promoter and enhancer. 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 melanocytes of the hair bulb and nonpigmented melanocytes of the hair bulge. The Donating Investigator reports that melanocyte stem cells from these mice do not produce CreERT2 after postnatal day 3. Mice that are hemizygous for the transgene are viable and fertile. Homozygous mice are reported to be lethal [October 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 (17&szlig;-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. Tg(Tyr-cre/ERT2)1Lru transgene insertion information: In October 2019, sequencing performed in the laboratory of Dr. Lionel Larue discovered that the Tg(Tyr-cre/ERT2)1Lru transgene inserted on the proximal end of chromosome 7 fused to a ~3 million base pair duplication from the proximal end of chromosome 2. This insertion also caused a deletion of some chromosome 7 loci. This insertion/deletion/duplication is characterized in <a href="https://www.ncbi.nlm.nih.gov/pubmed/31679174">Aktary et al. 2019 Pigment Cell Melanoma Res</a>. (see Figure 2a). Specifically, the insertion occurred on chromosome 7 into exon 10 of the Nlrp12 locus (3,220,560; mouse mm10), causing a deletion of centromeric sequences including the entire Speer9-ps1 and Au018091 loci as well as the remaining 3' Nlrp12 sequences. The duplicated chromosome 2 sequences (now fused to the transgene on chromosome 7) include the entire Fam171a1, Nmt2, Rpp38, Olah1, Meig1 and Dclre1c loci, as well as a portion of Suv39h2 lacking exons 1-2. Therefore, animals hemizygous for the Tg(Tyr-cre/ERT2)1Lru allele carry three copies of the duplicated chromosome 2 genes, but only one functional copy of the deleted chromosome 7 genes. Additionally, the investigators were unable to generate any animals homozygous for the transgene.

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Tyr::CreERT2 mice have expression of CreERT2 fusion protein directed by mouse tyrosinase promoter/enhancer regions. When bred with mice containing loxP-flanked sequences, tamoxifen/4-hydroxytamoxifen-inducible Cre-mediated recombination will result in deletion of the floxed sequences in the Tyr-expressing cells of the offspring. These mice are a Cre-lox tool that allows inducible Cre expression in melanoblasts and melanocytes. The Tg(Tyr-cre/ERT2)1Lru transgene inserted on the proximal end of chromosome 7 fused to a ~3 million base pair duplication from the proximal end of chromosome 2, also causing a deletion of some chromosome 7 loci. See Detailed Description below for more information on this integration/deletion/duplication event.

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