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First published online July 27, 2006
doi: 10.1242/10.1242/dev.02486
1 Institute for Stem Cell Research, GSF, National Research Center for
Environment and Health, Ingolstädter Landstr.1, D-85764
Neuherberg/Munich, Germany.
2 IGBMC, CNRS/INSERM/ULP, BP 163, 67404 Illkirch, CU de Strasbourg,
France.
3 Biomedical Research Centre, School of Biological Sciences, University of East
Anglia, Norwich, UK.
4 Department of Physiology, Ludwig-Maximilians University, Munich, Schillerstr.
46, D-80336, Munich, Germany.
* Author for correspondence at address 1 (e-mail: magdalena.goetz{at}gsf.de)
Accepted 12 June 2006
Radial glial cells have been shown to act as neuronal precursors in the
developing cortex and to maintain their radial processes attached to the
basement membrane (BM) during cell division. Here, we examined a potential
role of direct signalling from the BM to radial glial cells in three mouse
mutants where radial glia attachment to the BM is disrupted. This is the case
if the nidogen-binding site of the laminin 
1 chain is mutated, in the
absence of 
6 integrin or of perlecan, an essential BM component.
Surprisingly, cortical radial glial cells lacking contact to the BM were not
affected in their proliferation, interkinetic nuclear migration, orientation
of cell division and neurogenesis. Only a small subset of precursors was
located ectopically within the cortical parenchyma. Notably, however, neuronal
subtype composition was severely disturbed at late developmental stages (E18)
in the cortex of the laminin 1III4-/- mice. Thus, although
BM attachment seems dispensable for precursor cells, an intact BM is required
for adequate neuronal composition of the cerebral cortex.
Key words: Mouse, Basement membrane, Laminin, Cerebral cortex, Lamc1, Itaga6, Hspg2
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