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    The interaction between CASK and the tumour suppressor Dlg1 regulates mitotic spindle orientation in mammalian epithelia

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    Authors
    Porter, Andrew P
    White, Gavin R M
    Mack, Natalie A
    Malliri, Angeliki
    Affiliation
    Cell Signalling Group, Cancer Research UK Manchester Institute, The University of Manchester, Alderley Park, Macclesfield SK10 4TG, UK
    Issue Date
    2019
    
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    Show full item record
    Abstract
    Oriented cell divisions are important for the formation of normal epithelial structures. Dlg1, a tumour suppressor, is required for mitotic spindle orientation in Drosophila epithelia and chick neuroepithelia, but how Dlg1 is localised to the membrane and its importance in mammalian epithelia are unknown. We show that Dlg1 is required in non-transformed mammalian epithelial cells for oriented cell divisions and normal lumen formation. We demonstrate that the MAGUK protein CASK, a membrane-associated scaffold, is the factor responsible for Dlg1 membrane localisation during spindle orientation, thereby identifying a new cellular function for CASK. Depletion of CASK leads to misoriented divisions in 3D, and to the formation of multilumen structures in cultured kidney and breast epithelial cells. Blocking the CASK-Dlg1 interaction with an interfering peptide, or by deletion of the CASK-interaction domain of Dlg1, disrupts spindle orientation and causes multilumen formation. We show that the CASK-Dlg1 interaction is important for localisation of the canonical LGN-NuMA complex known to be required for spindle orientation. These results establish the importance of the CASK-Dlg1 interaction in oriented cell division and epithelial integrity.This article has an associated First Person interview with the first author of the paper.
    Citation
    Porter AP, White GRM, Mack NA, Malliri A. The interaction between CASK and the tumour suppressor Dlg1 regulates mitotic spindle orientation in mammalian epithelia. J Cell Sci. 2019 Jul 15;132(14).
    Journal
    Journal of Cell Science
    URI
    http://hdl.handle.net/10541/621985
    DOI
    10.1242/jcs.230086
    PubMed ID
    31289196
    Additional Links
    https://dx.doi.org/10.1242/jcs.230086
    Type
    Article
    Language
    en
    ae974a485f413a2113503eed53cd6c53
    10.1242/jcs.230086
    Scopus Count
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    All Paterson Institute for Cancer Research

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