These transgenic mice have a tamoxifen inducible Cre-mediated recombination system driven by the mouse neurogenin 1, Neurog1, 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/ESR1 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. Tamoxifen administration induces Cre recombination in the cortex, hippocampus, thalamus, hypothalamus and cochlear-vestibular ganglion. Hemizygous mutant mice are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Homozygotes are not viable. This mutant mouse strain may be useful for studying neuron development and lineage mapping of Neurog1 expressing cells.
In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an allele was first characterized. This is the case for the strain above. It should be noted that the phenotype could vary from that originally described. We will modify the strain description if necessary as published results become available.

When these Ngn1-CreERT2 transgenic mice are bred with mice containing a loxP-flanked sequence of interest, tamoxifen-inducible, Cre-mediated recombination will result in deletion of the flanked sequences in Neurog1 expressing cells such as neurons in the cortex, hippocampus, thalamus, hypothalamus and the cochlear-vestibular ganglion. This mutant mouse strain may be useful for studying neuron development and lineage mapping of Neurog1 expressing cells.

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