Cajal-Retzius cells (CRs) are peculiar neurons in the developing mammalian cerebral cortex. They robustly secrete Reln, a glycoprotein essential for the establishment of cortical layers through the control of radial migration. We previously identified Gmnc as a crucial fate determinant for P73+ CR subtypes. In Gmnc-/- mutants, P73+ CRs are initially produced and cover the telencephalic vesicle but undergo massive apoptosis resulting in their complete depletion at mid-corticogenesis. Here, we investigated the consequences of such a CR depletion on dorsal cortex lamination and hippocampal morphogenesis. We found that preplate splitting normally occurs in Gmnc-/- mutants but is followed by defective radial migration arrest in the dorsal cortex, an altered cellular organization in the lateral cortex, aberrant hippocampal CA1 folding and lack of vasculature development in the hippocampal fissure. We then performed conditional Reln deletion in P73+ CRs to evaluate its relative contribution and found that only radial migration defects were recapitulated. We concluded that at mid-corticogenesis, CR-derived Reln is required for radial migration arrest and additionally identified Reln-independent functions for CRs in the control of hippocampal fissure formation and CA1 folding.
Keywords: Cajal-Retzius cells; Cerebral Cortex; Hippocampus; Migration; Morphogenesis; Mouse.
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