A role for Bicaudal-D2 in radial cerebellar granule cell migration

Dick Jaarsma, Robert van den Berg, Phebe S. Wulf, Susan van Erp, Nanda Keijzer, Max A. Schlager, Esther de Graaff, Chris I. De Zeeuw, R. Jeroen Pasterkamp, Anna Akhmanova and Casper C. Hoogenraad ()
Additional contact information
Dick Jaarsma: Erasmus Medical Center
Robert van den Berg: Erasmus Medical Center
Phebe S. Wulf: Erasmus Medical Center
Susan van Erp: Netherlands Institute for Neuroscience, Royal Dutch Academy of Arts & Sciences
Nanda Keijzer: Erasmus Medical Center
Max A. Schlager: Erasmus Medical Center
Esther de Graaff: Erasmus Medical Center
Chris I. De Zeeuw: Erasmus Medical Center
R. Jeroen Pasterkamp: Brain Center Rudolf Magnus, University Medical Center Utrecht
Anna Akhmanova: Cell Biology, Faculty of Science, Utrecht University
Casper C. Hoogenraad: Erasmus Medical Center

Nature Communications, 2014, vol. 5, issue 1, 1-13

Abstract: Abstract Bicaudal-D (BICD) belongs to an evolutionary conserved family of dynein adaptor proteins. It was first described in Drosophila as an essential factor in fly oogenesis and embryogenesis. Missense mutations in a human BICD homologue, BICD2, have been linked to a dominant mild early onset form of spinal muscular atrophy. Here we further examine the in vivo function of BICD2 in Bicd2 knockout mice. BICD2-deficient mice develop disrupted laminar organization of cerebral cortex and the cerebellum, pointing to impaired radial neuronal migration. Using astrocyte and granule cell specific inactivation of BICD2, we show that the cerebellar migration defect is entirely dependent upon BICD2 expression in Bergmann glia cells. Proteomics analysis reveals that Bicd2 mutant mice have an altered composition of extracellular matrix proteins produced by glia cells. These findings demonstrate an essential non-cell-autonomous role of BICD2 in neuronal cell migration, which might be connected to cargo trafficking pathways in glia cells.

Date: 2014
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DOI: 10.1038/ncomms4411

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