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    Protocadherin 15 suppresses oligodendrocyte progenitor cell proliferation and promotes motility through distinct signalling pathways.

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    Author
    Zhen, Yilan
    Cullen, Carlie L
    Ricci, Raphael
    Summers, Benjamin S
    Rehman, Sakina
    Ahmed, Zubair M
    Foster, Antoinette Y
    Emery, Ben
    Gasperini, Robert
    Young, Kaylene M
    Date
    2022-05-30
    Journal
    Communications Biology
    Publisher
    Springer Nature
    Type
    Article
    
    Metadata
    Show full item record
    See at
    https://doi.org/10.1038/s42003-022-03470-1
    Data Availibility
    The associated raw video and image files are a research resource that will be made available by the corresponding author, upon reasonable request.
    Sponsors
    Oligodendrocyte progenitor cells (OPCs) express protocadherin 15 (Pcdh15), a member of the cadherin superfamily of transmembrane proteins. Little is known about the function of Pcdh15 in the central nervous system (CNS), however, Pcdh15 expression can predict glioma aggression and promote the separation of embryonic human OPCs immediately following a cell division. Herein, we show that Pcdh15 knockdown significantly increases extracellular signal-related kinase (ERK) phosphorylation and activation to enhance OPC proliferation in vitro. Furthermore, Pcdh15 knockdown elevates Cdc42-Arp2/3 signalling and impairs actin kinetics, reducing the frequency of lamellipodial extrusion and slowing filopodial withdrawal. Pcdh15 knockdown also reduces the number of processes supported by each OPC and new process generation. Our data indicate that Pcdh15 is a critical regulator of OPC proliferation and process motility, behaviours that characterise the function of these cells in the healthy CNS, and provide mechanistic insight into the role that Pcdh15 might play in glioma progression.
    Rights/Terms
    © 2022. The Author(s).
    Identifier to cite or link to this item
    http://hdl.handle.net/10713/19048
    ae974a485f413a2113503eed53cd6c53
    10.1038/s42003-022-03470-1
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