An apical MRCK-driven morphogenetic pathway controls epithelial polarity

Ceniz Zihni, Evi Vlassaks, Stephen Terry, Jeremy Carlton, Thomas King Chor Leung, Michael Olson, Franck Pichaud, Maria Susana Balda, Karl Matter

Research output: Contribution to journalArticlepeer-review


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.

Original languageEnglish
Pages (from-to)1049-1060
Number of pages12
JournalNature Cell Biology
Issue number9
Early online date21 Aug 2017
Publication statusPublished - 2017


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