Fig. 2

Disruption of the Akirin2 gene results in loss of the cerebral cortex. a A coronal section of the telencephalon of an Emx1-Cre; Ai14-tdTomato E12 embryo confirms the restriction of floxed allele excision to the dorsal (dCx) and lateral (lCx) cortex; Sytox Green is used as a cellular counterstain. b, c Low (b) and higher (c) magnification views of in situ hybridization utilizing Akirin2 probes on E11 telencephalon. Loss of Akirin2 begins in the dorsal cortex (arrows mark similar positions on two different E11 sections showing tdTomato Cre reporter fluorescence and antisense Akirin2 staining); some Akirin2 expression is still detected in the lateral cortex at this stage, but is not observed later as Cre activity expands (b). In knockout cortex at E11, Akirin2 antisense signal is reduced compared to controls, and is nearing background sense probe levels (c). d Akirin2 knockout causes severe microcephaly, which is already apparent by E12 and which leads to little, if any, remaining cortex in perinatal animals and in the rare animals that survive past P0 (one such knockout that survived to P22 is shown). e Cresyl violet staining of a rare surviving Akirin2 knockout and its littermate control at P16. There is no identifiable cortex or hippocampus in the knockout brain, though ventral structures appear to be present (note, for example, the prominent mammillary bodies in the lower right image). f Quantitative RT-PCR of control and Akirin2 knockout E15 forebrain RNA using a Taqman probe set for Emx1. Transcripts are nearly absent in the knockout tissue, consistent with loss of the cortex. ****p < 0.0001. LGE, lateral ganglionic eminence; LV, lateral ventricle. Scale bar: 200 μm in (a); 200 μm in (b); 100 μm in (c); 1 mm in (e)