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Published on: March 9, 2010
Myosin-dependent junction remodelling controls planar cell intercalation and axis elongation
Claire Bertet1, Lawrence Sulak, Thomas Lecuit
1Laboratoire de Génétique et de Physiologie du Développement, Institut de Biologie du Développement de Marseille, CNRS-INSERM-Université de la Méditerranée, Campus de Luminy, case 907, 13288 Marseille cedex 9, France.
Cell intercalation drives epithelial morphogenesis by reorganizing cell junctions. Myosin II activity is crucial for this process, providing a general model for tissue development.
Area of Science:
- Developmental biology
- Cell biology
- Biophysics
Background:
- Tissue shaping (morphogenesis) relies on cell division, shape, and neighbor changes via intercalation.
- Epithelial integrity, maintained by adherens junctions, presents unique challenges for intercalation.
Purpose of the Study:
- To elucidate the mechanism of ordered cell intercalation driving polarized epithelial morphogenesis.
- To understand the role of cell junctions and forces in germ-band elongation in Drosophila embryos.
Main Methods:
- Investigated junction remodeling during cell intercalation in Drosophila embryos.
- Analyzed the role of local forces and myosin II in planar junction remodeling.
Main Results:
- Cell intercalation progresses through spatial reorganization of adherens junctions.
- Planar junction remodeling is driven by local forces, not external tissue forces.
- Myosin II, enriched in disassembling junctions, is essential for planar remodeling and intercalation.
Conclusions:
- A novel cellular mechanism for polarized epithelial morphogenesis is proposed.
- Local forces and myosin II-dependent junction remodeling drive cell intercalation.
- This mechanism offers a general model for epithelial organ development.
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