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Updated: Jun 6, 2026
10:45
Analysis of Actomyosin Dynamics at Local Cellular and Tissue Scales Using Time-lapse Movies of Cultured Drosophila Egg Chambers
Published on: June 3, 2019
Planar polarized actomyosin contractile flows control epithelial junction remodelling.
Matteo Rauzi1, Pierre-François Lenne, Thomas Lecuit
1IBDML, UMR6216 CNRS-Université de la Méditerranée, Campus de Luminy, case 907, 13288 Marseille Cedex 09, France.
Nature
|November 12, 2010
Summary
Epithelial cell remodeling relies on myosin II (an actomyosin network) flowing towards junctions, not just static myosin. This flow is guided by E-cadherin distribution, driving tissue elongation in Drosophila embryos.
Area of Science:
- Cell Biology
- Developmental Biology
- Biophysics
Background:
- Myosin-II motors generate forces crucial for cell and tissue morphogenesis.
- Epithelial junctions, reinforced by E-cadherin, resist contractile forces and transmit tension.
- Drosophila embryonic germband extension involves cell intercalation and planar polarized remodeling of epithelial junctions.
Purpose of the Study:
- Investigate the interplay between force generation and cortical force transmission in epithelial cell deformation.
- Clarify the mechanism driving the shrinkage of dorsal-ventral-oriented junctions during Drosophila germband extension.
- Determine the role of myosin II distribution and actomyosin flow in epithelial morphogenesis.
Main Methods:
- Utilized Drosophila melanogaster as a model organism.
- Investigated junctional remodeling and cell deformations during embryonic germband extension.
- Analyzed the role of myosin II, E-cadherin, and α-Catenin in force transmission and actomyosin dynamics.
Main Results:
- Junctional shrinkage is driven by polarized flow of medial actomyosin pulses towards dorsal-ventral junctions, not by junctional myosin II.
- Anisotropic actomyosin flow is oriented by the planar polarized distribution of E-cadherin complexes.
- Medial myosin II flows towards junctions with less E-cadherin, suggesting an equilibrium property of force transmission and E-cadherin coupling via α-Catenin.
Conclusions:
- Epithelial morphogenesis is regulated by polarized contractile actomyosin flows, not solely by myosin II steady-state distribution.
- The interaction between E-cadherin and actomyosin networks dictates the medial flow pattern.
- This study reveals a novel mechanism for force transmission and tissue remodeling in epithelia.
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