The secreted BMP (bone morphogenic protein) antagonist encoded by the Grem1 gene is a marker for skeletal stem cells. These transgenic mice express a tamoxifen-inducible Cre recombinase driven by the mouse Grem1 promoter. The transgene insert contains a fusion product involving Cre recombinase and a mutant form of the human estrogen receptor ligand binding domain. The mutant human 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, the offspring are useful for generating tamoxifen-induced, Cre-mediated targeted deletions of the flanked sequence. Tamoxifen administration in double mutant mice, carrying this transgene, induces Cre recombination in Grem1 expressing cells. The Donating Investigator reports that homozygotes are viable. During backcrossing, the Y chromosome may not have been fixed to the C57BL/6J genetic background.

These Grem1-creERT mice express a tamoxifen-inducible Cre recombinase under the control of the mouse Grem1 promoter. When bred with mice containing loxP-flanked sequences, tamoxifen-inducible Cre-mediated recombination will result in deletion of the floxed sequences in the Grem1-expressing cells of the offspring. These mice may be useful for generating conditional mutations for studying gain or loss of function and/or fate mapping in bone marrow osteochondroreticular stem cells (skeletal stem cells), and intestinal reticular stem cells.

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B6.Cg-Tg(Grem1-cre/ERT)3Tcw/J Frozen Embryo