Disruption of the gene in zebrafish reveals conserved functions in development of the craniofacial skeleton and the thyroid.

Mutations in the FOXE1 gene are implicated in cleft palate and thyroid dysgenesis in humans. To investigate whether zebrafish could provide meaningful insights into the etiology of developmental defects in humans related to FOXE1, we generated a zebrafish mutant that has a disruption in the nuclear localization signal in the foxe1 gene, thereby restraining nuclear access of the transcription factor. We characterized skeletal development and thyroidogenesis in these mutants, focusing on embryonic and larval stages.