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PMID: 9856459 Published · ppublish English Journal Article Research Support, Non-U.S. Gov't

Pax6 controls radial glia differentiation in the cerebral cortex.

Neuron ·Vol. 21 ·No. 5 ·1998-11-00 ·Pages 1031-44

Götz M, Stoykova A, Gruss P

Abstract

Radial glia cells perform a dual function in the developing nervous system as precursor cells and guides for migrating neurons. We show here that during forebrain neurogenesis, the transcription factor Pax6 is specifically localized in radial glia cells of the cortex but not of the basal telencephalon. In Pax6-deficient mice, cortical radial glia cells were altered in their morphology, number, tenascin-C (TN-C) expression, and cell cycle. We show that some of these alterations are cell-autonomous, whereas others were rescued by coculturing with wild-type cortical cells. Our results suggest that Pax6 plays an essential role in the differentiation of cortical radial glia. Thus, despite their widespread distribution, radial glia cells are regionally specified in the developing CNS.

MeSH Terms
Animals Cell Differentiation/genetics Cells, Cultured Cerebral Cortex/cytology,growth & development,pathology DNA-Binding Proteins/genetics,physiology Embryo, Mammalian Eye Proteins Growth Substances/physiology Homeodomain Proteins Mice Mice, Inbred C57BL Mice, Knockout Mice, Mutant Strains Mutation Neuroglia/cytology,metabolism,pathology PAX6 Transcription Factor Paired Box Transcription Factors Repressor Proteins Stem Cells/metabolism
Chemicals
DNA-Binding Proteins Eye Proteins Growth Substances Homeodomain Proteins PAX6 Transcription Factor Paired Box Transcription Factors Pax6 protein, mouse Repressor Proteins
Authors & Affiliations
3 authors, click to expand affiliations / ORCID
Götz M
Department of Molecular Cell Biology, Max-Planck Institute of Biophysical Chemistry, Göttingen, Federal Republic of Germany.
Stoykova A
Gruss P
Article Info
Journal
Neuron
Abbr.
Neuron
ISSN
0896-6273
Published
1998-11-00
Pages
1031-44
Language
English
Region
United States
NLM ID
8809320
Subset
IM
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