These brn3a-CreERT2 transgenic mice express a tamoxifen inducible Cre recombinase driven by the 11kb mouse Pou4f1 (POU domain, class 4, transcription factor 1) gene promoter. The transgene insert contains a fusion product involving Cre recombinase and a mutant form of the mouse estrogen receptor ligand binding domain. The mutant mouse estrogen receptor does not bind natural ligand at physiological concentrations but will bind the synthetic ligand, 4-hydroxytamoxifen. Restricted to the cytoplasm, the cre/ERT2 protein can only gain access to the nuclear compartment after exposure to tamoxifen. 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 in Pou4f1-expressing tissues. Tamoxifen administration induces Cre recombination in sensory neurons. Inducible Cre recombinase activity is detected in adult DRG (dorsal root ganglion) neurons. Preliminary crosses suggest that homozygotes may not 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 (17&beta;-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. &nbsp;

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brn3a-CreERT2 transgenic mice have the mouse Pou4f1 gene promoter directing expression of tamoxifen-inducible Cre recombinase, and may be useful for mediating inducible Cre recombination in Pou4f1-expressing tissues, including sensory neurons.

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