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Publication Detail
An apical MRCK-driven morphogenetic pathway controls epithelial polarity.
  • Publication Type:
    Journal article
  • Publication Sub Type:
    Article
  • Authors:
    Zihni C, Vlassaks E, Terry S, Carlton J, Leung TKC, Olson M, Pichaud F, Balda MS, Matter K
  • Publication date:
    01/09/2017
  • Journal:
    Nature cell biology
  • Medium:
    Print-Electronic
  • Print ISSN:
    1465-7392
  • Language:
    eng
  • Addresses:
    Institute of Ophthalmology, University College London, Bath Street, London EC1V 9EL, UK.
Abstract
Polarized epithelia develop distinct cell surface domains, with the apical membrane acquiring characteristic morphological features such as microvilli. Cell polarization is driven by polarity determinants including the evolutionarily conserved partitioning-defective (PAR) proteins that are separated into distinct cortical domains. PAR protein segregation is thought to be a consequence of asymmetric actomyosin contractions. The mechanism of activation of apically polarized actomyosin contractility is unknown. Here we show that the Cdc42 effector MRCK activates myosin-II at the apical pole to segregate aPKC-Par6 from junctional Par3, defining the apical domain. Apically polarized MRCK-activated actomyosin contractility is reinforced by cooperation with aPKC-Par6 downregulating antagonistic RhoA-driven junctional actomyosin contractility, and drives polarization of cytosolic brush border determinants and apical morphogenesis. MRCK-activated polarized actomyosin contractility is required for apical differentiation and morphogenesis in vertebrate epithelia and Drosophila photoreceptors. Our results identify an apical origin of actomyosin-driven morphogenesis that couples cytoskeletal reorganization to PAR polarity signalling.
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Institute of Ophthalmology
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Institute of Ophthalmology
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Lab for Molecular Cell Bio MRC-UCL
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The Ear Institute
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Institute of Ophthalmology
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