Planar polarized actomyosin contractile flows control epithelial junction remodelling

• Published in: Nature (London) 2010-12, Vol.468 (7327), p.1110-1114
• Main Authors: Rauzi, Matteo, Lenne, Pierre-François, Lecuit, Thomas
• Format: Article
• Language: English
• Subjects: 631/136/1660; 631/80/128; 631/80/79/2028; Actomyosin - metabolism; Animals; Anisotropy; Biological and medical sciences; Cadherins - metabolism; Cell Polarity; Cellular Biology; Deformation; Drosophila melanogaster - cytology; Drosophila melanogaster - embryology; Drosophila Proteins - metabolism; Embryo, Nonmammalian - cytology; Embryo, Nonmammalian - embryology; Embryology: invertebrates and vertebrates. Teratology; Epithelial Cells - cytology; Epithelial Cells - metabolism; Flow pattern; Fundamental and applied biological sciences. Psychology; Humanities and Social Sciences; Insects; Intercellular Junctions - metabolism; letter; Life Sciences; Morphology; multidisciplinary; Myosin Type II - metabolism; Organogenesis. Fetal development; Organogenesis. Physiological fonctions; Protein Transport; Science; Science (multidisciplinary)
• ISSN: 0028-0836; 1476-4687
• DOI: 10.1038/nature09566

Myosin-II in epithelial morphogenesis Myosin-II has a central role in generating the forces that drive cell shape changes during embryo development. Thomas Lecuit and colleagues study germ-band extension in Drosophila , in which epithelial cells undergo an ordered process of intercalation resulting in tissue extension through remodelling of cell junctions. They find that cell-junction shrinkage is driven by polarized flow of medial myosin-II pulses towards junctions, which organizes the whole process of intercalation. In addition, the flow of myosin-II is driven by the polarized distribution of E-cadherin/β-catenin/ α-catenin complexes at adherens junctions. Thus, epithelial morphogenesis is driven by polarized contractile actomyosin flows emerging from interactions between E-cadherin and actomyosin networks. Here, germ-band extension in Drosophila is studied in which epithelial cells undergo an ordered process of intercalation resulting in tissue extension through remodelling of cell junctions. Cell junction shrinkage is driven by polarized flow of medial Myosin-II pulses towards junctions which organizes the whole process of intercalation. The flow of Myosin II is driven by the polarized distribution of E-cadherin complexes at adherens junctions. Thus, epithelial morphogenesis is driven by polarized contractile actomyosin flows emerging from interactions between E-cadherin and actomyosin networks. Force generation by Myosin-II motors on actin filaments drives cell and tissue morphogenesis 1 , 2 , 3 , 4 , 5 , 6 , 7 , 8 , 9 , 10 , 11 , 12 , 13 , 14 , 15 . In epithelia, contractile forces are resisted at apical junctions by adhesive forces dependent on E-cadherin 16 , which also transmits tension 6 , 17 , 18 , 19 . During Drosophila embryonic germband extension, tissue elongation is driven by cell intercalation 20 , which requires an irreversible and planar polarized remodelling of epithelial cell junctions 4 , 5 . We investigate how cell deformations emerge from the interplay between force generation and cortical force transmission during this remodelling in Drosophila melanogaster . The shrinkage of dorsal–ventral-oriented (‘vertical’) junctions during this process is known to require planar polarized junctional contractility by Myosin II (refs 4 , 5 , 7 , 12 ). Here we show that this shrinkage is not produced by junctional Myosin II itself, but by the polarized flow of medial actomyosin pulses towards ‘vertical’ junctions. This anisotropic flow is orient