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The Journal of Neuroscience, February 1, 2000, 20(3):1109-1118

The Lack of Emx2 Causes Impairment of Reelin Signaling and Defects of Neuronal Migration in the Developing Cerebral Cortex

Antonello Mallamaci¹, Sara Mercurio¹, Luca Muzio¹, Chiara Cecchi¹, Celia Leonor Pardini¹, Peter Gruss², and Edoardo Boncinelli^{1, 3}

¹ Department of Biological and Technological Research (DIBIT), Istituto Scientifico H. San Raffaele, 20132 Milano, Italy, ² Max-Planck Institute of Biophysical Chemistry, 37018 Goettingen, Germany, and ³ Molecular and Cellular Pharmacology, Consiglio Nazionale delle Ricerche, 20129 Milano, Italy

Neocorticogenesis in mice homozygous for an Emx2 null allele is the topic of this article. The development of both main components of neocortex, primordial plexiform layer derivatives and cortical plate, was analyzed, paying special attention to radial migration of neurons forming the cortical plate. The products of the Reelin gene, normally playing a key role in orchestrating radial migration of these neurons, display normal distribution at the beginning of the cortical neuronogenesis but are absent in the neocortical marginal zone of the mutant mice at the time when the cortical plate is laid down. As a consequence, the development of radial glia is impaired, and neurons making up the cortical plate display abnormal migration patterns. In addition, restricted defects along the rostrocaudal and the mediolateral axes are present in the subplate, suggesting an Emx2-specific role in priming the proper development of this layer.

Key words: neocortex; Emx2; Cajal-Retzius cells; reeler; radial glia; subplate

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Copyright © 2000 Society for Neuroscience  0270-6474/00/2031109-10$05.00/0

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