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The lack of Emx2 causes impairment of Reelin signaling and defects of neuronal migration in the developing cerebral cortex.
Mallamaci, A; Mercurio, S; Muzio, L; Cecchi, C; Pardini, C L; Gruss, P; Boncinelli, E.
Afiliación
  • Mallamaci A; Department of Biological and Technological Research (DIBIT), Istituto Scientifico H. San Raffaele, 20132 Milano, Italy. mallamaci.antonio@hsr.it
J Neurosci ; 20(3): 1109-18, 2000 Feb 01.
Article en En | MEDLINE | ID: mdl-10648716
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.
Asunto(s)

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Transducción de Señal / Moléculas de Adhesión Celular Neuronal / Corteza Cerebral / Proteínas de la Matriz Extracelular / Proteínas de Homeodominio / Neuronas Tipo de estudio: Etiology_studies Límite: Animals Idioma: En Revista: J Neurosci Año: 2000 Tipo del documento: Article País de afiliación: Italia Pais de publicación: Estados Unidos

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Transducción de Señal / Moléculas de Adhesión Celular Neuronal / Corteza Cerebral / Proteínas de la Matriz Extracelular / Proteínas de Homeodominio / Neuronas Tipo de estudio: Etiology_studies Límite: Animals Idioma: En Revista: J Neurosci Año: 2000 Tipo del documento: Article País de afiliación: Italia Pais de publicación: Estados Unidos