Btbd7 (BTB (POZ) domain containing 7), induced by fibronectin, regulates epithelial cell dynamics and branching morphogenesis which are involved with embryonic organogenesis. It is a critical regulator of cleft formation during in vitro branching morphogenesis that functions via the downregulation of E-cadherin and stimulation of epithelial cell motility. Btbd7 also promotes an epithelial-to-mesenchymal transition in cultured tumor cells, with an increase in invasive capability.

Exons 3 and 4 of the mouse Btbd7 gene are flanked by loxP sites in this conditional mutant strain. Cre-mediated excision of the floxed region produces a knock-out allele. 

Widespread knock-out of Btbd7, achieved through crosses with CMV-cre mice (see Stock No. <a href="https://www.jax.org/strain/006054"">006054</a>), causes severe inhibition of embryonic salivary gland, lung, and kidney organ formation due to inhibition of branching morphogenesis. There are no apparent effects on pancreas and heart development, which are known to use different mechanisms. Homozygous knock-out mice are not viable. Ex vivo and in vitro studies have established that Btbd7 has roles in enhancing rates of cell migration, suppressing levels of the cell-cell adhesion molecule E-cadherin, and promoting cell scattering and branching morphogenesis in a process of partial epithelial-mesenchymal transition (EMT; tumor budding).

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Exons 3 and 4 of the mouse Btbd7 gene are flanked by loxP sites in this conditional mutant strain. Cre-mediated excision of the floxed region produce a knock-out allele useful in studies of endothelial cell dynamics and embryonic organogenesis.

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