TY - JOUR
T1 - β1-Class integrins regulate the development of laminae and folia in the cerebral and cerebellar cortex
AU - Graus-Porta, Diana
AU - Blaess, Sandra
AU - Senften, Mathias
AU - Littlewood-Evans, Amanda
AU - Damsky, Caroline
AU - Huang, Zhen
AU - Orban, Paul
AU - Klein, Rüdiger
AU - Schittny, Johannes C.
AU - Müller, Ulrich
N1 - Funding Information:
We thank Louis F. Reichardt for his support; A.M. Goffinet, A. Matus, D. Monard, and L. Sorokin for antibodies; S. Orkin for lacZ-loxP tester mice; members of the laboratory for discussions; J.F. Spetz and P. Kopp for help with generating mice; S. Fumagalli, D. Monard, A. Matus, A. Kralli, and Louis F. Reichardt for reading of the manuscript; and M. Frotscher for discussions. This work was initiated in the laboratory of Louis F. Reichardt, where it was supported by United States Public Health Service grant NS19090. The work was subsequently supported by the Novartis Research Foundation. S.B. was supported by the Roche Research Foundation; D.G. and U.M. received a grant from the Swiss Foundation for Research on Muscular Disease. L.F.R. is an investigator of the Howard Hughes Medical Institute.
PY - 2001/8/16
Y1 - 2001/8/16
N2 - Mice that lack all β1-class integrins in neurons and glia die prematurely after birth with severe brain malformations. Cortical hemispheres and cerebellar folia fuse, and cortical laminae are perturbed. These defects result from disorganization of the cortical marginal zone, where β1-class integrins regulate glial endfeet anchorage, meningeal basement membrane remodeling, and formation of the Cajal-Retzius cell layer. Surprisingly, β1-class integrins are not essential for neuron-glia interactions and neuronal migration during corticogenesis. The phenotype of the β1-deficient mice resembles pathological changes observed in human cortical dysplasias, suggesting that defective integrin-mediated signal transduction contributes to the development of some of these diseases.
AB - Mice that lack all β1-class integrins in neurons and glia die prematurely after birth with severe brain malformations. Cortical hemispheres and cerebellar folia fuse, and cortical laminae are perturbed. These defects result from disorganization of the cortical marginal zone, where β1-class integrins regulate glial endfeet anchorage, meningeal basement membrane remodeling, and formation of the Cajal-Retzius cell layer. Surprisingly, β1-class integrins are not essential for neuron-glia interactions and neuronal migration during corticogenesis. The phenotype of the β1-deficient mice resembles pathological changes observed in human cortical dysplasias, suggesting that defective integrin-mediated signal transduction contributes to the development of some of these diseases.
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U2 - 10.1016/S0896-6273(01)00374-9
DO - 10.1016/S0896-6273(01)00374-9
M3 - Article
C2 - 11516395
AN - SCOPUS:17944373768
SN - 0896-6273
VL - 31
SP - 367
EP - 379
JO - Neuron
JF - Neuron
IS - 3
ER -