Lamination of the cerebral cortex is disturbed in Gli3 mutant mice

• Published in: Developmental biology 2008-06, Vol.318 (1), p.203-214
• Main Authors: Friedrichs, Melanie, Larralde, Osmany, Skutella, Thomas, Theil, Thomas
• Format: Article
• Language: English
• Subjects: Animals; Axin Protein; Biomarkers - metabolism; Cell Adhesion Molecules, Neuronal - genetics; Cell Adhesion Molecules, Neuronal - metabolism; Cerebral cortex; Cerebral Cortex - anatomy & histology; Cerebral Cortex - embryology; Cerebral Cortex - metabolism; Cytoskeletal Proteins - genetics; Cytoskeletal Proteins - metabolism; Embryo, Mammalian - anatomy & histology; Embryo, Mammalian - physiology; Extracellular Matrix Proteins - genetics; Extracellular Matrix Proteins - metabolism; Gli3; Humans; In Situ Hybridization; Kruppel-Like Transcription Factors - genetics; Kruppel-Like Transcription Factors - metabolism; Lamination; Mice; Mutation; Nerve Tissue Proteins - genetics; Nerve Tissue Proteins - metabolism; Neurons - cytology; Neurons - metabolism; Reelin; Serine Endopeptidases - genetics; Serine Endopeptidases - metabolism; Zinc Finger Protein Gli3
• ISSN: 0012-1606; 1095-564X
• DOI: 10.1016/j.ydbio.2008.03.032

The layered organization of the cerebral cortex develops in an inside-out pattern, a process which is controlled by the secreted protein reelin. Here we report on cortical lamination in the Gli3 hypomorphic mouse mutant Xt J/ Pdn which lacks the cortical hem, a major source of reelin + Cajal Retzius cells in the cerebral cortex. Unlike other previously described mouse mutants with hem defects, cortical lamination is disturbed in Xt J/ Pdn animals. Surprisingly, these layering defects occur in the presence of reelin + cells which are probably derived from an expanded Dbx1 + progenitor pool in the mutant. However, while these reelin + neurons and also Calretinin + cells are initially evenly distributed over the cortical surface they form clusters later during development suggesting a novel role for Gli3 in maintaining the proper arrangement of these cells in the marginal zone. Moreover, the radial glial network is disturbed in the regions of these clusters. In addition, the differentiation of subplate cells is affected which serve as a framework for developing a properly laminated cortex.