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Using floxed \u03b2\u2010catenin gain\u2010of\u2010function (GOF) and loss\u2010of\u2010function (LOF) alleles, we found <jats:italic>Tbx1<\/jats:italic> expression was down\u2010regulated and maintained\/enhanced in the two mouse mutants, respectively. <jats:italic>Bmp4<\/jats:italic> was ectopically expressed and <jats:italic>Otx1<\/jats:italic> was lost in \u03b2\u2010catenin GOF mutants. Normally, inactivation of <jats:italic>Tbx1<\/jats:italic> causes expanded neurogenesis, but expression of <jats:italic>NeuroD<\/jats:italic> was down\u2010regulated in \u03b2\u2010catenin GOF mutants. To explain this paradox, <jats:italic>Eya1<\/jats:italic> and <jats:italic>Six1<\/jats:italic>, genes for branchio\u2010oto\u2010renal (BOR) syndrome were down\u2010regulated in the OV of \u03b2\u2010catenin GOF mutants independently of <jats:italic>Tbx1<\/jats:italic>. Overall, this work helps explain the mechanism by which Wnt signaling modulates transcription factors required for neurogenesis and patterning of the OV. Developmental Dynamics 239:1708\u20131722, 2010. \u00a9 2010 Wiley\u2010Liss, Inc.<\/jats:p>","DOI":"10.1002\/dvdy.22308","type":"journal-article","created":{"date-parts":[[2010,5,12]],"date-time":"2010-05-12T14:00:32Z","timestamp":1273672832000},"page":"1708-1722","source":"Crossref","is-referenced-by-count":41,"title":["Canonical Wnt signaling modulates <i>Tbx1<\/i>, <i>Eya1<\/i>, and <i>Six1<\/i> expression, restricting neurogenesis in the otic vesicle"],"prefix":"10.1002","volume":"239","author":[{"given":"Laina","family":"Freyer","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Bernice 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