Canonical Wnt signaling is not required for expression in the basal medial edge epithelium during palatogenesis.

The secondary palate forms from two lateral primordia called the palatal shelves which form a contact in the midline, become adherent at the fusing interface (medial edge epithelia, MEE) and subsequently fuse. The gene encoding transforming growth factor-ß3 () is strongly and specifically expressed in MEE cells. Our previous study suggested that expression is controlled via upstream cis-regulatory elements in and around the neighboring gene. Another study suggested that the canonical Wnt signaling via ß-Catenin is responsible for the MEE-specific gene expression, since deletion of the gene by a commonly used Keratin 14-Cre () mouse line almost completely abolished expression in the MEE resulting in cleft palate. Here, we wanted to analyze whether consensus binding sites located in the previously identified regions of the gene are responsible for the spatiotemporal control of expression during palatogenesis. We show that contrary to the previous report, deletion of the gene in basal MEE cells by the driver (the same mouse line was used as in the previous study referenced above) does not affect the MEE-specific expression or TGFß3-dependent palatal epithelial fusion. All mutant embryos showed a lack of palatal rugae accompanied by other craniofacial defects, e.g., a narrow snout and a small upper lip, while only a small subset (<5%) of mutants displayed a cleft palate. Moreover, the embryos showed reduced levels and altered patterns of expression. Our present data imply that epithelial ß-catenin may not be required for MEE-specific expression or palatal epithelial fusion.