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The corpus callosum (CC) represents the major forebrain commissure connecting the 2 cerebral hemispheres. Midline crossing of callosal axons is controlled by several glial and neuronal guideposts specifically located along the callosal path, but it remains unknown how these cells acquire their position. Here, we show that the  Gli3  hypomorphic mouse mutant  Polydactyly Nagoya  ( Pdn ) displays agenesis of the CC and mislocation of the glial and neuronal guidepost cells. Using transplantation experiments, we demonstrate that agenesis of the CC is primarily caused by midline defects. These defects originate during telencephalic patterning and involve an up-regulation of  Slit2  expression and altered Fgf and Wnt/β-catenin signaling. Mutations in  sprouty1/2  which mimic the changes in these signaling pathways cause a disorganization of midline guideposts and CC agenesis. Moreover, a partial recovery of midline abnormalities in  Pdn/Pdn ; Slit2  − / −  embryos mutants confirms the functional importance of correct  Slit2  expression levels for callosal development. Hence,  Gli3  controlled restriction of Fgf and Wnt/β-catenin signaling and of  Slit2  expression is crucial for positioning midline guideposts and callosal development.

Gli3 Controls Corpus Callosum Formation by Positioning Midline Guideposts During Telencephalic Patterning