Ap2

**Abstract(s):** Failure of facial prominence fusion causes cleft lip and palate (CL/P), a common human birth defect. Several potential mechanisms can be envisioned that would result in CL/P, including failure of prominence growth and/or alignment as well as a failure of fusion of the juxtaposed epithelial seams. Here, the authors analyzed facial outgrowth and shape change over time in a novel mouse model exhibiting fully penetrant bilateral CL/P. This robust model is based upon mutations in Tfap2a, the gene encoding transcription factor AP-2α, which has been implicated in both syndromic and non-syndromic human CL/P. **Gene(s):** [Tfap2a](https://www.alliancegenome.org/gene/MGI:104671): Enables several functions, including DNA-binding transcription factor activity, RNA polymerase II-specific; transcription coactivator activity; and transcription corepressor activity. Involved in several processes, including camera-type eye development; cranial nerve development; and regulation of gene expression. Acts upstream of or within several processes, including animal organ development; embryonic morphogenesis; and face morphogenesis. Located in clathrin-coated pit and nucleus. Is expressed in several structures, including branchial arch; genitourinary system; limb; nervous system; and sensory organ. Used to study orofacial cleft. Human ortholog(s) of this gene implicated in branchiooculofacial syndrome. Orthologous to human TFAP2A (transcription factor AP-2 alpha).