Fig. 5: Agenesis of the corpus callosum in Celsr1 KO mice.

a, b Representative images of the hippocampal commissure phenotype. Coronal sections stained with Cresyl Echt Violet (Nissl bodies, a) or Luxol Fast Blue (Myelin, b) from adult control (Celsr1 wildtype, left) (Ctrl) and Celsr1 KO mice (right). Note the absence of the corpus callosum in the KO. c Coronal sections from control (left) and Celsr1 KO (right) newborn mice were immunostained with Tag1 (green) to show pioneer callosal axons, and GFAP (magenta) to reveal glial cells involved in the midline crossing of these axons. Tag1 immunostaining, showed that callosal axons fail to cross the midline and run along the rostral-caudal axis, forming the Probst bundles (pb). Glial cells of the indusium griseum (IG, magenta) were absent in the KO. The glial wedge that expresses GFAP and behaves as a repulsive cue towards extending axons, although present, showed a wider interhemispheric spacing. d Representative images of DiI tracing. Callosal axons could be traced to the contralateral hemisphere in the control, but not in the KO mice. Lower panels in (c, d) show higher magnifications of the boxed areas in the corresponding upper panels. Callosal pioneer axons fail to project to the contralateral hemisphere in the KO mouse. Observations without quantification have been validated and successfully reproduced in a minimum of three different animals. Scale bars, (a, b) 500 µm, (c, d) 500 µm upper panels, 200 µm bottom panels. AC anterior commissure, CC corpus callosum, Cx cortex, DG dentate gyrus, GW glial wedge, HC hippocampus, IG indusium griseum, pb Probst bundles. Uncropped and unprocessed data are available as Supplementary Fig. 5.