作者: S. Pompolo , V.R. Harley
DOI: 10.1016/S0006-8993(01)02574-4
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摘要: Human mutations in the transcription factor gene, SOX9, cause campomelic dysplasia (CD), a severe dwarfism associated with brain abnormalities including dilation of lateral ventricles, hypoplasia corpus callosum and cerebellum defects. To improve our understanding how SOX9 contributes to molecular genetic pathway development we sought investigate distribution protein rat mouse brain. The regions expression identified this study correlated sites reported CD patients. immunoreactivity was observed nuclei scattered cells throughout brain, ependymal layer choroid plexus. In forebrain most SOX9-immunoreactive co-localised glial astrocyte marker S-100. cerebellum, mostly surrounding Purkinje cells, which were identified, by electron microscopy, as Golgi epithelial also known Bergmann glia. Using antibody for precursors glia, traced their origin during development. At embryonic day (E)14.5 E16.5, present mainly primordial plexus, ventricular zone. By E18.5, granular cell layers but no labelling detectable external layer. These results suggest that is favour proposed secondary scaffold arising from derived exclusively