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    Protrudin functions from the endoplasmic reticulum to support axon regeneration in the adult CNS.

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    Author
    Petrova, V; Pearson, CS; Ching, J; Tribble, JR; Solano, AG; Yang, Y; Love, FM; Watt, RJ; Osborne, A; Reid, E; ...
    Date
    2020-11-05
    Source Title
    Nature Communications
    Publisher
    Springer Science and Business Media LLC
    University of Melbourne Author/s
    Martin, Keith
    Affiliation
    Ophthalmology (Eye & Ear Hospital)
    Metadata
    Show full item record
    Document Type
    Journal Article
    Citations
    Petrova, V., Pearson, C. S., Ching, J., Tribble, J. R., Solano, A. G., Yang, Y., Love, F. M., Watt, R. J., Osborne, A., Reid, E., Williams, P. A., Martin, K. R., Geller, H. M., Eva, R. & Fawcett, J. W. (2020). Protrudin functions from the endoplasmic reticulum to support axon regeneration in the adult CNS.. Nat Commun, 11 (1), pp.5614-. https://doi.org/10.1038/s41467-020-19436-y.
    Access Status
    Open Access
    URI
    http://hdl.handle.net/11343/252265
    DOI
    10.1038/s41467-020-19436-y
    Open Access at PMC
    http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7645621
    Abstract
    Adult mammalian central nervous system axons have intrinsically poor regenerative capacity, so axonal injury has permanent consequences. One approach to enhancing regeneration is to increase the axonal supply of growth molecules and organelles. We achieved this by expressing the adaptor molecule Protrudin which is normally found at low levels in non-regenerative neurons. Elevated Protrudin expression enabled robust central nervous system regeneration both in vitro in primary cortical neurons and in vivo in the injured adult optic nerve. Protrudin overexpression facilitated the accumulation of endoplasmic reticulum, integrins and Rab11 endosomes in the distal axon, whilst removing Protrudin's endoplasmic reticulum localization, kinesin-binding or phosphoinositide-binding properties abrogated the regenerative effects. These results demonstrate that Protrudin promotes regeneration by functioning as a scaffold to link axonal organelles, motors and membranes, establishing important roles for these cellular components in mediating regeneration in the adult central nervous system.

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