Fig. 1.

Changes in telencephalon and cortical interneuron transcripts during OFC pathogenesis. a,b Representative vehicle-exposed control and cyclopamine-exposed OFC embryos at GD14.0. c,d ISH staining for Gli1 on parasagittal sections through the frontonasal prominence (FNP) of GD9.25 embryos illustrates reduced Shh-signaling activity during initial OFC pathogenesis. e,f Along with a scanning electron micrograph image of a GD9.25 mouse embryo, a schematic of a parasagittal section shows the cell populations comprising the FNP including the neuroectoderm (NE), facial mesenchyme (FM) and facial ectoderm (FE). (Right) Microarray analyses of microdissected FNP tissue from GD9.25 control versus OFC groups revealed differential expression of orofacial cleft, telencephalon, and cortical interneuron-related genes. V ventricle