The AP-2alphaki knock-in/knockout allele has an IRES-lacZ cassette inserted into exon 7 of the transcription factor AP-2α gene; both abolishing endogenous gene function and placing lacZ expression under direction of the Tfap2a promoter/enhancer regions. Wildtype mice have AP-2alpha expression in the neural tube, and in cranial and cardiac neural crest cells in the developing embryo, as well as in the progress zone of the limb bud, the developing kidney, the eye, and surface ectoderm. Most homozygotes exhibit prenatal or postnatal lethality due to neural tube, craniofacial, body wall, and cardiac malfomation, while the majority of heterozygotes are viable and fertile. In these mice, β-gal labels the ectoderm, and cranial and cardiac neural crest populations during the E8.5-10.5. Homozygous mice exhibit failure of neural tube closure by E9.5, and outflow tract abnormalities from E14.5-15.5.
