Fig. 3
From: Mutations in SMARCB1 and in other Coffin–Siris syndrome genes lead to various brain midline defects
Aberrant midline glia in mutant mice. a–j Immunostainings of P0 coronal brain sections: Neuropilin 1-positive cortical axons fail to cross horizontally in mutant animals. Instead, some axon bundles deviate ventrally at the ipsilateral side (arrows in h). Gfap-positive midline glia are aberrantly positioned and the glial wedge population is diminished in the mutant brain (g) GW glial wedge, IGG indusium griseum glia, MZG midline zipper glia. A widened interhemispheric fissure (IHF, laminin-positive connective tissue cells and basement membranes are stained in d and i) that is not crossed by cortical axons is present in the mutant brain. k, l Immunostainings of E18.5 coronal brain sections with an anti-Glast antibody (red immunosignals). The Glast-positive radial glial population at the position of the prospective Gfap-positive GW is reduced and shows shorter radial processes (arrowheads in k, l). Glast-positive immunosignals above the developing corpus callosum are horizontally positioned in the control brain (arrow in k) but deviate toward the midline in the mutant brain (arrow in l). All scale bars: 100 µm
