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 (Tgfb3) is strongly and specifically expressed in MEE cells. Our previous study suggested thatTgfb3expression is controlled via upstream cis-regulatory elements in and around the neighboringIft43gene. Another study suggested that the canonical Wnt signaling via ß-Catenin is responsible for the MEE-specificTgfb3gene expression, since deletion of theCtnnb1gene by a commonly used Keratin 14-Cre (K14Cre) mouse line almost completely abolishedTgfb3expression in the MEE resulting in cleft palate. Here, we wanted to analyze whetherTcf/Lefconsensus binding sites located in the previously identified regions of theIft43gene are responsible for the spatiotemporal control ofTgfb3expression during palatogenesis. We show that contrary to the previous report, deletion of theCtnnb1gene in basal MEE cells by theK14Credriver (the sameK14Cremouse line was used as in the previous study referenced above) does not affect the MEE-specificTgfb3expression 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%) ofCtnnb1mutants displayed a cleft palate. Moreover, theK14Cre:Ctnnb1embryos showed reduced levels and altered patterns ofShhexpression. Our present data imply that epithelial ß-catenin may not be required for MEE-specificTgfb3expression or palatal epithelial fusion.