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    TUBB5 and its disease-associated mutations influence the terminal differentiation and dendritic spine densities of cerebral cortical neurons

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    Authors
    Ngo, L.
    Haas, M.
    Qu, Z.
    Li, S.
    Zenker, J.
    Teng, K.
    Gunnersen, J.
    Breuss, M.
    Habgood, M.
    Keays, D.
    Heng, Julian
    Date
    2014
    Type
    Journal Article
    
    Metadata
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    Citation
    Ngo, L. and Haas, M. and Qu, Z. and Li, S. and Zenker, J. and Teng, K. and Gunnersen, J. et al. 2014. TUBB5 and its disease-associated mutations influence the terminal differentiation and dendritic spine densities of cerebral cortical neurons. Human Molecular Genetics. 23 (19): pp. 5147-5158.
    Source Title
    Human Molecular Genetics
    DOI
    10.1093/hmg/ddu238
    ISSN
    1460-2083
    School
    Health Sciences Research and Graduate Studies
    URI
    http://hdl.handle.net/20.500.11937/73072
    Collection
    • Curtin Research Publications
    Abstract

    © The Author 2014. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oup.com. The microtubule cytoskeleton is critical for the generation and maturation of neurons in the developing mammalian nervous system. We have previously shown that mutations in the ß-tubulin gene TUBB5 cause microcephaly with structural brain abnormalities in humans. While it is known that TUBB5 is necessary for the proper generation and migration of neurons, little is understood of the role it plays in neuronal differentiation and connectivity. Here, we report that perturbations to TUBB5 disrupt the morphology of cortical neurons, their neuronal complexity, axonal outgrowth, as well as the density and shape of dendritic spines in the postnatal murine cortex. The features we describe are consistent with defects in synaptic signaling. Cellular-based assays have revealed that TUBB5 substitutions have the capacity to alter the dynamic properties and polymerization rates of the microtubule cytoskeleton. Together, our studies show that TUBB5 is essential for neuronal differentiation and dendritic spine formation in vivo, providing insight into the underlying cellular pathology associated with TUBB5 disease states.

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