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An apical MRCK-driven morphogenetic pathway controls epithelial polarity.

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Myotonic dystrophy-related Cdc42-binding kinase (MRCK) activates apical actomyosin contractility, segregating polarity proteins and driving epithelial morphogenesis. This establishes an apical origin for cytoskeletal reorganization coupled with polarity signaling.

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Area of Science:

  • Cell Biology
  • Developmental Biology
  • Epithelial Biology

Background:

  • Polarized epithelia establish distinct apical and basolateral membrane domains crucial for tissue function.
  • Cell polarization is regulated by polarity determinants, including the evolutionarily conserved partitioning-defective (PAR) proteins.
  • PAR protein segregation is hypothesized to result from asymmetric actomyosin contractions, but the activation mechanism remains unclear.

Purpose of the Study:

  • To elucidate the mechanism of activation of apically polarized actomyosin contractility.
  • To identify the upstream regulators of apical actomyosin contractility and their role in cell polarization and morphogenesis.
  • To understand how cytoskeletal reorganization is coupled to PAR polarity signaling.

Main Methods:

  • Investigated the role of the Cdc42 effector Myotonic dystrophy-related Cdc42-binding kinase (MRCK) in epithelial cell polarization.
  • Utilized techniques to analyze actomyosin contractility, protein segregation, and cytoskeletal organization in polarized epithelia.
  • Examined the function of MRCK-activated contractility in apical differentiation and morphogenesis in vertebrate epithelia and Drosophila photoreceptors.

Main Results:

  • MRCK activates myosin-II at the apical pole, leading to the segregation of aPKC-Par6 from junctional Par3 and defining the apical domain.
  • Apically polarized MRCK-activated actomyosin contractility is reinforced by cooperation with aPKC-Par6, which downregulates antagonistic RhoA-driven junctional contractility.
  • This apical contractility drives the polarization of cytosolic brush border determinants and promotes apical morphogenesis.

Conclusions:

  • MRCK-activated polarized actomyosin contractility is essential for apical differentiation and morphogenesis in various epithelial systems.
  • This study reveals an apical origin of actomyosin-driven morphogenesis, linking cytoskeletal dynamics to PAR polarity signaling.
  • The findings provide a novel mechanism for how apical cell surface domains are established and maintained.