These transgenic mice have a tamoxifen inducible Cre-mediated recombination system driven by the mouse Dlx1/2, distal-less homeobox 1, distal-less homeobox 2, forebrain enhancer/ promoter (I12b). The transgene insert contains a fusion product involving Cre recombinase and a mutant form of the mouse estrogen receptor ligand binding domain, and the human placental alkaline phosphatase (ALPP or PLAP). 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/ESR1 protein can only gain access to the nuclear compartment after exposure to tamoxifen. When crossed with a strain containing loxP site flanked sequences, the flanked sequences will be deleted in the cre-expressing tissues in the offspring upon administration of tamoxifen. Tamoxifen administration induces Cre recombination in the ventral telencephalon and diencephalon as early as embryonic day 10.5 and in the olfactory bulb interneurons as early as embryonic day 15.5. Inducible recombinase activity occurs in olfactory bulb interneuron precursors throughout adulthood. The expression pattern of the transgene is similar to the endogenous forebrain expression pattern of Dlx1/2 as detected by alkaline phosphatase, placental (PLAP) histochemical analysis. Hemizygous mutant mice are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. The Donating Investigator has not attempted to make the strain homozygous.

These transgenic mice express a tamoxifen-inducible Cre recombinase under the control of the mouse I12b enhancer element of Dlx1/2, and may be useful for generating temporal conditional mutations for studying gain or loss of function and/or fate mapping in Dlx1/2-expressing forebrain tissues, including interneurons of the olfactory bulb and neocortex.

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