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NMII forms a contractile transcellular sarcomeric network to regulate apical cell junctions and tissue geometry.

Seham Ebrahim1, Tomoki Fujita, Bryan A Millis

  • 1Laboratory of Cell Structure and Dynamics, National Institute on Deafness and Other Communication Disorders, National Institutes of Health, Bethesda, MD 20892, USA.

Current Biology : CB
|April 9, 2013
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Nonmuscle myosin II (NMII) forms muscle-like sarcomeric units around epithelial cells. These paired sarcomeres create a transcellular contractile network, regulating cell shape and tissue tension.

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Area of Science:

  • Cell Biology
  • Biophysics
  • Developmental Biology

Background:

  • Nonmuscle myosin II (NMII) integrates force at epithelial apical junctions, crucial for tissue morphogenesis and homeostasis.
  • NMII dysfunction is linked to diseases involving cell-cell adhesion failures.
  • The precise organization and tension-generating mechanism of NMII at intercellular junctions remain unclear.

Purpose of the Study:

  • To elucidate the structural organization of NMII at epithelial junctions.
  • To understand how NMII generates and responds to tension along the intercellular junctional line.
  • To investigate the role of NMII in epithelial tissue organization and disease.

Main Methods:

  • High-resolution imaging of NMII organization within epithelial cells.
  • Analysis of actin and α-actinin interactions with NMII filaments.
  • Investigating the functional consequences of NMII sarcomere dynamics on cell and tissue shape.

Main Results:

  • Discovered periodic, muscle-like sarcomeric units of NMII filaments, actin, and α-actinin forming a continuous belt around epithelial cells.
  • Demonstrated precise pairing of these sarcomeres between adjacent cells, creating an integrated transcellular contractile network.
  • Observed that sarcomere contraction/relaxation directly influences apical cell shape and tissue geometry.
  • Showed differential distribution and isoform compensation of NMII at heterotypic junctions.

Conclusions:

  • Proposed a model for NMII force generation and transmission across epithelial cell junctions via paired sarcomeres.
  • Highlighted the sarcomeric network as a key regulator of epithelial organization, homeostasis, development, and disease.
  • Established a framework for investigating NMII's multifaceted roles in cell adhesion and tissue dynamics.