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Tracking Morphogenetic Tissue Deformations in the Early Chick Embryo
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A self-organized biomechanical network drives shape changes during tissue morphogenesis.

Akankshi Munjal1, Jean-Marc Philippe1, Edwin Munro2

  • 1Aix Marseille Université, CNRS, IBDM UMR7288, 13009 Marseille, France.

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|July 28, 2015
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Summary
This summary is machine-generated.

Cell shape changes during tissue morphogenesis are driven by non-muscle myosin II (MyoII) and actin. This study reveals how MyoII dynamics, regulated by the Rho1-Rok pathway, create stability and pulsatility for cell intercalation.

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Area of Science:

  • Cell Biology
  • Developmental Biology
  • Biophysics

Background:

  • Tissue morphogenesis relies on cell shape changes powered by actomyosin networks.
  • Non-muscle myosin II (MyoII) and filamentous actin (F-actin) form dynamic networks that drive cell deformations and stabilization.
  • The precise mechanisms governing the pulsatility and stability of actomyosin networks remain unclear.

Purpose of the Study:

  • To investigate the role of the Rho1-Rok pathway in regulating MyoII dynamics during Drosophila melanogaster germband extension.
  • To elucidate the mechanisms underlying the stability and pulsatility of actomyosin networks during cell intercalation.

Main Methods:

  • Utilized Drosophila melanogaster as a model organism.
  • Investigated the Rho1-Rok pathway's role in MyoII regulation.
  • Analyzed MyoII dynamics, including exchange kinetics and advection, through phosphorylation-dephosphorylation cycles and motor contraction on F-actin networks.

Main Results:

  • Identified two critical properties of MyoII dynamics: exchange kinetics and advection, which govern stability and pulsatility.
  • Demonstrated that spatial control over MyoII exchange kinetics establishes stable regimes of high and low dissociation rates, leading to MyoII planar polarity.
  • Showed that pulsatility emerges at intermediate dissociation rates, facilitating the advection of MyoII and its regulators, and is a self-organized process driven by biomechanical feedback.

Conclusions:

  • MyoII dynamics, specifically exchange kinetics and advection, are crucial for generating both stability and pulsatility during tissue morphogenesis.
  • The Rho1-Rok pathway spatially regulates MyoII dynamics, establishing planar polarity and enabling pulsatile contractions essential for cell intercalation.
  • Actomyosin pulsatility is a self-organized phenomenon arising from biomechanical feedback, rather than an upstream pacemaker.