Fig. 7

Disruption of the cortical hem in the absence of Akirin2. In situ hybridization for a number of cortical patterning genes at E10.5 (a, d), E11 (b, e) and E13 (c) is shown. The cortical hem, a medial structure that releases Wnt signaling molecules to pattern the cortex, is disrupted in Akirin2 knockouts, as few if any Wnt3a or Wnt5a transcripts are detected (a, b). Consistent with this, the Wnt-responsive genes Lef1 and Dmrt3 are reduced or absent in the knockout cortex (a, b). The transthyretin (TTR)-positive choroid plexus, and the ventromedial domain of Fgf8 expression, both of which are wholly or partially spared by Emx1-Cre, remain present in the knockout (c), though the location of the choroid plexus is shifted dorsally due to the loss of cortical tissue. Expression patterns of the proneural transcription factors Ngn2 and Lhx2 appear fairly normal in the dorsal cortical region, although the loss of tissue documented previously is observed at E11 (d, e). Arrows represent the region of Emx1-Cre activity at E10.5 and E11, identified by tdTomato reporter boundaries in other sections not shown. Black arrowheads show the Wnt3a and Wnt5a-positive cortical hem and red arrowheads show the TTR-positive choroid plexus. Scale bar: 200 μm in (a, b, d, e); 300 μm in (c)