The extracellular signaling factor encoded by Wnt4 (wingless-type MMTV integration site family, member 4) plays an important role in the mesenchyme-to-epithelial transition during nephron development.
The Wnt4GCE knock-in/knock-out allele both abolishes Wnt4 gene function and expresses an eGFPCreERT2 fusion protein (EGFP and creERT2 fusion protein) from the Wnt4 promoter/enhancer elements. Inducible Cre recombinase activity is detected in nephron tubule cells outside the cortical region at 19.5 dpc, after tamoxifen injection at 12.5 dpc. GFP expression is detected in developing nephron tubules at 15.5 dpc. Heterozygous mice are viable and fertile. Homozygous viability/fertility has not been tested (August 2018)- the Donating Investigator does not expect homozygotes to 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.

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These mice harbor a Wnt4GCE knock-in/knock-out allele that both abolishes Wnt4 gene function and expresses EGFP and creERT2 from the Wnt4 promoter/enhancer elements. While EGFP expression is observed in developing nephron tubules at 15.5 dpc, Cre-ERT2 fusion gene activity is observed in the same cells only following tamoxifen administration. These Wnt4GCE mice may be useful for lineage-tracing/marking Wnt4-expressing during kidney organogenesis.

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