Basolateral protrusion and apical contraction cooperatively drive Drosophila germ-band extension

• Published in: Nature cell biology Vol. 19; no. 4; pp. 375 - 383
• Main Authors: Sun, Zijun, Amourda, Christopher, Shagirov, Murat, Hara, Yusuke, Saunders, Timothy E., Toyama, Yusuke
• Format: Journal Article
• Language: English
• Published: London Nature Publishing Group UK 01.04.2017; Nature Publishing Group
• Subjects: 14/19; 14/35; 14/69; 631/136/2434; 631/136/334/1582/715; 631/80/84; 64/24; Actin; Actins - metabolism; Animals; Body Patterning; Cancer Research; Cell adhesion & migration; Cell Biology; Cell migration; Cell Polarity; Contractility; Contraction; Cytological research; Developmental Biology; Drosophila; Drosophila melanogaster - cytology; Drosophila melanogaster - embryology; Drosophila Proteins - metabolism; Embryo, Nonmammalian - cytology; Insects; Intercalation; letter; Life Sciences; Mechanics (physics); Microscopy, Fluorescence, Multiphoton; Myosin; Observations; Phosphatidylinositol Phosphates - metabolism; rac GTP-Binding Proteins - metabolism; Rac1 protein; Rosette formation; Stem Cells; Time-Lapse Imaging
• ISSN: 1465-7392; 1476-4679
• DOI: 10.1038/ncb3497

Sun  et al.  show that during Drosophila germ-band extension basolateral rosette formation does not depend on apical contractility, but is driven by Rac1-mediated protrusion and active cell migration and requires Src42A as a regulator. Throughout development, tissues undergo complex morphological changes, resulting from cellular mechanics that evolve over time and in three-dimensional space. During Drosophila germ-band extension (GBE), cell intercalation is the key mechanism for tissue extension 1 , and the associated apical junction remodelling is driven by polarized myosin-II-dependent contraction 2 , 3 , 4 . However, the contribution of the basolateral cellular mechanics to GBE remains poorly understood. Here, we characterize how cells coordinate their shape from the apical to the basal side during rosette formation, a hallmark of cell intercalation. Basolateral rosette formation is driven by cells mostly located at the dorsal/ventral part of the rosette (D/V cells). These cells exhibit actin-rich wedge-shaped basolateral protrusions and migrate towards each other. Surprisingly, the formation of basolateral rosettes precedes that of the apical rosettes. Basolateral rosette formation is independent of apical contractility, but requires Rac1-dependent protrusive motility. Furthermore, we identified Src42A as a regulator of basolateral rosette formation. Our data show that in addition to apical contraction, active cell migration driven by basolateral protrusions plays a pivotal role in rosette formation and contributes to GBE.