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Many ASDs are thought to involve an inappropriate patterning and migration of the periocular mesenchyme (POM), which is derived from cranial neural crest cells (NCC) and mesoderm. Although, the mechanism of this disruption is not well understood a number of transcriptional regulatory molecules have previously been implicated in ASDs. Here we investigate the function of the transcription factor AP-2\u03b2, encoded by Tfap2b, which is expressed in the NCC and its derivatives. Wnt1-Cre mediated conditional deletion of Tfap2b in NCC resulted in postnatal ocular defects typified by opacity. Histological data revealed that the conditional AP-2\u03b2 NCC knockout mutants exhibited dysgenesis of multiple structures in the anterior segment of the eye including defects in the corneal endothelium, corneal stroma, ciliary body and disruption in the iridocorneal angle with adherence of the iris to the cornea. We further show that this phenotype leads to a significant increase in intraocular pressure and a subsequent loss of retinal ganglion cells and optic nerve degeneration, features indicative of glaucoma. Overall, our findings demonstrate that AP-2\u03b2 is required in the POM for normal development of the anterior segment of the eye and that the AP-2\u03b2 NCC KO mice may serve as a new and exciting model of ASD and glaucoma that is fully penetrant and with early post-natal onset.<\/jats:p>","DOI":"10.1242\/dmm.025262","type":"journal-article","created":{"date-parts":[[2016,6,24]],"date-time":"2016-06-24T02:02:58Z","timestamp":1466733778000},"source":"Crossref","is-referenced-by-count":23,"title":["Conditional deletion of AP-2\u03b2 in the cranial neural crest results in anterior segment dysgenesis and early-onset glaucoma"],"prefix":"10.1242","author":[{"given":"Vanessa B.","family":"Martino","sequence":"first","affiliation":[{"name":"Department of Pathology and Molecular Medicine, McMaster University Health Science Centre, Rm 1R10, 1200 Main St. West. 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