Figure 3

Distribution of tangentially migrating cells analyzed by RNA in situ hybridization. (A-H) Coronal sections of WT (A-D) and Foxc1^hith/hith (E-H) embryos at E17.5. Expression of Cxcl12 in the mutant appears fragmented in dorsal aspects and unaffected in ventrolateral aspects of the meninges (E). Expression of cortical interneuron markers Lhx6 and Gad67, although continuous in the WT (B, C), is absent in dorsal aspects of the cortical marginal zone in the mutant (G, H). The loss of expression of these two markers in the MZ starts exactly at the level where Cxcl12 expression breaks down as indicated by red arrowheads. Interestingly, expression of Lhx6 is increased and widened in the dorsal SVZ of the mutant (F, yellow asterisk), consistent with the β-gal expression results from Figure 1. Expression of Reln, which marks CRCs appears continuous in the WT (D) but is mildly disrupted in the dorsal aspect of the mutant (H). The breakup of continuous Reln expression occurs at the same lateral position as Cxcl12 disruption (red arrowhead) but appears less fragmented than Cxcl12 expression. Gaps in Reln expression in the MZ are indicated by red asterisks (H). A close-up of the dorsal cortex in a homozygote mutant shows double RNA in situ hybridization analysis for Cxcl12 and Reln (H'), confirming the expression of Cxcl12 by CRCs. All Cxcl12+ cells are also positive for the expression of Reln. Note also that some Reln+ cells do not express Cxcl12 (red arrowhead). Scale bars: 200 μm (A-H); 20 μm (H'). Cx, cerebral cortex; HC, hippocampus; Me, meninges; ML, midline; Th, thalamus.