Fig. 3
From: Early dorsomedial tissue interactions regulate gyrification of distal neocortex
Dual loss of complementary expressed Lmx1a/b causes transient DMe mispatterning. a, b In situ stained wild-type coronal telencephalic sections at e10.5 showing specific expression of Lmx1a in the DMe and Lmx1b—in medial mesenchyme (mes.). c–f At e12.5, wild-type CH expressed Wnt3a (c), while ChPe—Ttr (e). In Lmx1a−/−;b−/− mutants, Wnt3a expression domain was enlarged, expanding into the prospective ChPe territory (d, arrowhead), while Ttr was not expressed (f, arrowhead). g–j DMe patterning was restored in e15.5 Lmx1a−/−;b−/− mutants, with Ttr expression in the ChPe and Wnt3a—in the CH. Wnt3a+ CH domain, however, was abnormally small (g, h). Scale bars: 200 μm (a, b, g, h); 150 μm (c–f); 250 μm (i, j)
