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Letters to Nature
Nature 429, 667-671 (10 June 2004) | doi:10.1038/nature02590; Received 27 February 2004; Accepted 23 April 2004
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Gastroenterologist
- Wayne State University
- Detroit, Michigan, USA
Assistant Professor and Associate Professor
- Massachusetts General Hospital/ Harvard Medical School
- Charlestown, MA
Myosin-dependent junction remodelling controls planar cell intercalation and axis elongation
Claire Bertet, Lawrence Sulak & Thomas Lecuit
- Laboratoire de Génétique et de Physiologie du Développement (LGPD), Institut de Biologie du Développement de Marseille (IBDM), CNRS-INSERM-Université de la Méditerranée, Campus de Luminy, case 907, 13288 Marseille cedex 9, France
Correspondence to: Thomas Lecuit Email: lecuit@ibdm.univ-mrs.fr
Abstract
Shaping a developing organ or embryo relies on the spatial regulation of cell division and shape. However, morphogenesis also occurs through changes in cell-neighbourhood relationships produced by intercalation1, 2. Intercalation poses a special problem in epithelia because of the adherens junctions, which maintain the integrity of the tissue. Here we address the mechanism by which an ordered process of cell intercalation directs polarized epithelial morphogenesis during germ-band elongation, the developmental elongation of the Drosophila embryo. Intercalation progresses because junctions are spatially reorganized in the plane of the epithelium following an ordered pattern of disassembly and reassembly. The planar remodelling of junctions is not driven by external forces at the tissue boundaries but depends on local forces at cell boundaries. Myosin II is specifically enriched in disassembling junctions, and its planar polarized localization and activity are required for planar junction remodelling and cell intercalation. This simple cellular mechanism provides a general model for polarized morphogenesis in epithelial organs.
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