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The Journal of Neuroscience, December 1, 1998, 18(23):9858-9869
Evidence for the Participation of the Neuron-Specific CDK5 Activator P35 during Laminin-Enhanced Axonal Growth
Gabriela Paglini1, Gustavo Pigino1, Patricia Kunda1, Gerardo Morfini1, Ricardo Maccioni2, Santiago Quiroga3, Adriana Ferreira4, and Alfredo Cáceres1 1 Instituto Mercedes y Martín Ferreyra, Consejo Nacional de Investigaciones Científicas y Técnicas (CONICET), 5000 Cordoba, Argentina, 2 Laboratorio Biología Celular y Molecular, Universidad de Chile, 5000 Santiago, Chile, 3 Departamento Quimica Biologica, CONICET, Universidad Nacional de Cordoba, 5000 Cordoba, Argentina, and 4 Institute of Neuroscience and Department of Cell and Molecular Biology, Northwestern University, Chicago, Illinois 60611
Cultures of cerebellar macroneurons were used to study the pattern of expression, subcellular localization, and function of the neuronal cdk5 activator p35 during laminin-enhanced axonal growth. The results obtained indicate that laminin, an extracellular matrix molecule capable of selectively stimulating axonal extension and promoting MAP1B phosphorylation at a proline-directed protein kinase epitope, selectively stimulates p35 expression, increases its association with the subcortical cytoskeleton, and accelerates its redistribution to the axonal growth cones. Besides, suppression of p35, but not of a highly related isoform designated as p39, by antisense oligonucleotide treatment selectively reduces cdk5 activity, laminin-enhanced axonal elongation, and MAP1b phosphorylation. Taken collectively, the present results suggest that cdk5/p35 may serve as an important regulatory linker between environmental signals (e.g., laminin) and constituents of the intracellular machinery (e.g., MAP1B) involved in axonal elongation.
Key words: cdk5; p35; neurons; development; axon; growth cones; MAP1b; phosphorylation; antisense oligonucleotides; neuronal cultures
Copyright © 1998 Society for Neuroscience 0270-6474/98/18239858-12$05.00/0
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