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The Journal of Neuroscience, March 31, 2004, 24(13):3402-3412; doi:10.1523/JNEUROSCI.5241-03.2004
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Development/Plasticity/Repair
 1-Integrins Are Critical for Cerebellar Granule Cell Precursor Proliferation
Sandra Blaess,1 *
Diana Graus-Porta,2 *
Richard Belvindrah,3
Randor Radakovits,3
Sebastian Pons,4
Amanda Littlewood-Evans,2
Mathias Senften,3
Huailian Guo,5
Yuqing Li,5
Jeffrey H. Miner,6
Louis F. Reichardt,7 and
Ulrich Müller3
1Howard Hughes Medical Institute and Developmental Genetics Program, Skirball Institute of Biomolecular Medicine, New York University School of Medicine, New York, New York 10016, 2Novartis Institutes for BioMedical Research, Novartis Pharma AG, 4002 Basel, CH, Switzerland, 3The Scripps Research Institute, Department of Cell Biology, Institute for Childhood and Neglected Disease, La Jolla, California 92037, 4Instituto de Investigaciones Biomedidicas de Barcelona, Consejo Superior de Investigaciones Científicas, Barcelona 08036, Spain, 5Department of Molecular and Integrative Physiology, Neuroscience Program and Beckman Institute of Advanced Science and Technology, Urbana, Illinois 61801, 6Renal Division, Washington University School of Medicine, St. Louis, Missouri 63110, and 7Department of Physiology and Howard Hughes Medical Institute, University of California, San Francisco, California 94143-0723
We have previously shown that mice with a CNS restricted knock-out of the integrin  1 subunit gene (Itgb1-CNSko mice) have defects in the formation of lamina and folia in the cerebral and cerebellar cortices that are caused by disruption of the cortical marginal zones. Cortical structures in postnatal and adult Itgb1-CNSko animals are also reduced in size, but the mechanism that causes the size defect has remained unclear. We now demonstrate that proliferation of granule cell precursors (GCPs) is severely affected in the developing cerebellum of Itgb1-CNSko mice. In the absence of 1 expression, GCPs lose contact with laminin in the meningeal basement membrane, cease proliferating, and differentiate prematurely. In vitro studies provide evidence that1 integrins act at least in part cell autonomously in GCPs to regulate their proliferation. Previous studies have shown that sonic hedgehog (Shh)-induced GCP proliferation is potentiated by the integrin ligand laminin. We show that Shh directly binds to laminin and that laminin–Shh induced cell proliferation is dependent on 1 integrin expression in GCPs. Taken together, these data are consistent with a model in which 1 integrin expression in GCPs is required to recruit a laminin–Shh complex to the surface of GCPs and to subsequently modulate the activity of signaling pathways that regulate proliferation.
Key words: integrin; laminin; sonic hedgehog; proliferation; granule cell precursor
Received Nov 26, 2003;
revised February 6, 2004;
accepted February 13, 2004.
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