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SCRIB controls apical contractility during epithelial differentiation

Batiste Boëda1, Vincent Michel2, Raphael Etournay3

  • 1Cell Polarity, Migration and Cancer Unit, Université Paris Cité, UMR3691 CNRS, Institut Pasteur, Paris, France.

The Journal of Cell Biology
|November 6, 2023
PubMed

Insights

SCRIB gene mutations cause organ defects. Our study reveals SCRIB controls gut epithelial shape by regulating apical contractility during cell differentiation, impacting myosin light chain activity.

Area of Science:

  • Cell Biology
  • Developmental Biology
  • Genetics

Background:

  • Mutations in the SCRIB gene are linked to diverse morphological organ defects in vertebrates.
  • The precise molecular mechanisms connecting SCRIB to organ shape determination are not fully understood.

Purpose of the Study:

  • To investigate the role of SCRIB in the morphogenesis of gut epithelium using an organ-on-chip model.
  • To elucidate the molecular pathways influenced by SCRIB during epithelial development.

Main Methods:

  • Utilized an organ-on-chip model to study SCRIB knockout (KO) gut-like epithelia.
  • Performed cell differentiation assays on filters to analyze apical cell shape and polarity.
  • Investigated the molecular interactions of SCRIB with SHROOM2/4 and ROCK1.

Main Results:

  • SCRIB KO epithelia exhibited a flatter morphology with a reduced apical surface area.
  • SCRIB is essential for controlling apical cell shape and basoapical polarization of myosin light chain localization and activity.
  • Identified a conserved SHROOM binding site in SCRIB required for its function in apical cell shape regulation.

Conclusions:

  • SCRIB is a critical regulator of epithelial morphogenesis.
  • SCRIB controls epithelial apical contractility during cell differentiation through interactions with SHROOM2/4 and ROCK1.

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