A role of MAP1B in reelin-dependent neuronal migration

Gonzalez-Billault, C; Jimenez-Mateos E.M.; Wandosell F.; Avila J.; Del Rio J.A.; Urena J.M.; Barallobre M.J.; Pascual, M; Pujadas L.; Simo S.; La Torre A.; Gavin R.; Soriano, E

Keywords: proteins, system, neurons, adhesion, enzyme, mouse, activation, animals, phosphorylation, movement, brain, protein, cell, gene, microtubule, pregnancy, matrix, synthase, mice, embryo, experiment, transduction, transgenic, migration, deletion, nerve, tissue, reelin, female, signal, rna, cortex, neuronal, article, kinase, translation, correlation, analysis, function, malformation, glycogen, controlled, animal, study, 3, cyclin, priority, nonhuman, journal, Nervous, serine, Cells,, Cultured, associated, Mice,, Cerebral, extracellular, 5, dependent, Microtubule-Associated, Endopeptidases, Molecules,

Abstract

The signaling cascades governing neuronal migration are believed to link extracellular signals to cytoskeletal components. MAP1B is a neuron-specific microtubule-associated protein implicated in the control of the dynamic stability of microtubules and in the cross-talk between microtubules and actin filaments. Here we show that Reelin can induce mode I MAP1B phosphorylation, both in vivo and in vitro, through gsk3 and cdk5 activation. Additionally, mDab1 participates in the signaling cascade responsible for mode I MAP1B phosphorylation. Conversely, MAP1B-deficient mice display an abnormal structuring of the nervous system, especially in brain laminated areas, indicating a failure in neuronal migration. Therefore, we propose that Reelin can induce post-translational modifications on MAP1B that could correlate with its function in neuronal migration. © Oxford University Press 2004; all rights reserved.

Más información

Título de la Revista: CEREBRAL CORTEX
Volumen: 15
Número: 8
Editorial: OXFORD UNIV PRESS INC
Fecha de publicación: 2005
Página de inicio: 1134
Página final: 1145
URL: http://www.scopus.com/inward/record.url?eid=2-s2.0-25444431830&partnerID=q2rCbXpz