Fig. 1

Defects in development of major axon tracts and migration of interneurons in the Foxg1-Cre;Rac1 ^CKO/− forebrain. a–c’ Neurofilament (NF) immunostaining of coronal brain sections at E18.5 shows an enlarged lateral ventricle (encircled by a white line), absence of multiple axon tracts, and misrouting of thalamocortical axons in the embryonic Foxg1-Cre;Rac1 ^CKO/− brain. In the Foxg1-Cre;Rac1 ^CKO/− brain, corticospinal axons are partially obscured by misrouted thalamocortical axons. Numbered white arrows (control) and arrowheads (mutant) point to corresponding axon tracts: 1, axons in the cortical intermediate zone; 2, corpus callosum; 3, axons in the striatum; 4, anterior commissure; 5, thalamocortical axons; and 6, corticospinal tract. N = 2 for each genotype. In this and all other figures, images are shown from a representative embryo of the indicated genotype. Scale bar, 500 μm. d–g’ Calbindin immunostaining of E13.5 sections shows the absence of calbindin⁺ interneurons in the Foxg1-Cre;Rac1 ^CKO/− neocortex. e, e’, g, g’ are enlarged views of boxed regions in (d, d’, f, f’), respectively. In the WT neocortex, interneurons (green arrows) exhibit elongated bipolar morphology parallel to the plane of the cortex, indicative of tangential migration. In the Foxg1-Cre;Rac1 ^CKO/− forebrain, calbindin⁺ interneurons are seen in the ventral telencephalon but are not found in the neocortex. The lateral ventricle is already enlarged by this stage. Faint background immunostaining is present in the vasculature. CGE caudal ganglionic eminence, LGE lateral ganglionic eminence, MGE medial ganglionic eminence. N = 3 for each genotype. Scale bars: d’, 500 μm; g’, 100 μm. h–j’ Neurofilament (NF) immunostaining of coronal Rac1 ^CKO/+ vs. Foxg1-Cre;Rac1 ^CKO/+ ;Fz3 ^+/− brain sections at E18.5. The corpus callosum is indicated by a white arrow in (h, i). The corresponding non-crossing fibers are indicated by a white arrowhead in (h’, i’). N = 2 for each genotype. Scale bar, 500 μm. k Planes of sections in (a–g’)