Dynamic features of adherens junctions during Drosophila embryonic epithelial morphogenesis revealed by a D α-catenin-GFP fusion protein

Oda, Hiroki; Tsukita, Shöichiro

doi:10.1007/s004270050246

Cited by 66 publications

(51 citation statements)

References 19 publications

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“…Consistent with this model is the observation that E-cadherin transcription is repressed by Snail and N-cadherin transcription is upregulated by Twist (Oda and Tsukita, 1999). However, N-cadherin protein accumulates in the mesoderm only at later stages during monolayer formation (Oda and Tsukita, 1999). We find that throughout mesoderm spreading, the maternally provided E-cadherin remains present in mesoderm cells (Fig.…”

Section: Research Articlesupporting

confidence: 84%

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Fibroblast growth factor signalling controls successive cell behaviours during mesoderm layer formation in Drosophila

et al. 2011

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SUMMARYFibroblast growth factor (FGF)-dependent epithelial-mesenchymal transitions and cell migration contribute to the establishment of germ layers in vertebrates and other animals, but a comprehensive demonstration of the cellular activities that FGF controls to mediate these events has not been provided for any system. The establishment of the Drosophila mesoderm layer from an epithelial primordium involves a transition to a mesenchymal state and the dispersal of cells away from the site of internalisation in a FGF-dependent fashion. We show here that FGF plays multiple roles at successive stages of mesoderm morphogenesis in Drosophila. It is first required for the mesoderm primordium to lose its epithelial polarity. An intimate, FGF-dependent contact is established and maintained between the germ layers through mesoderm cell protrusions. These protrusions extend deep into the underlying ectoderm epithelium and are associated with high levels of E-cadherin at the germ layer interface. Finally, FGF directs distinct hitherto unrecognised and partially redundant protrusive behaviours during later mesoderm spreading. Cells first move radially towards the ectoderm, and then switch to a dorsally directed movement across its surface. We show that both movements are important for layer formation and present evidence suggesting that they are controlled by genetically distinct mechanisms.

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Section: Research Articlesupporting

confidence: 84%

“…It has been suggested that ME separation represents a classic example of tissue separation via differential expression of cadherins (Oda and Tsukita, 1999). Consistent with this model is the observation that E-cadherin transcription is repressed by Snail and N-cadherin transcription is upregulated by Twist (Oda and Tsukita, 1999).…”

Section: Research Articlementioning

confidence: 74%

Fibroblast growth factor signalling controls successive cell behaviours during mesoderm layer formation in Drosophila

et al. 2011

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“…The Drosophila stocks UbiDE-Cadherin GFP (38) (from T. Uemura, Kyoto, Japan), Histone H2B EGFP, sqh GFP (39) (from J. Raff, Oxford, UK), and UAS-Apoliner (Bloomington Stock Center) were used to constitutively mark apical membranes at the level of adherens junctions, nuclei, nonmuscle myosin II RLC, and caspase activity, respectively. Recombinants of maternal α-tubulin Gal4 and UAS EB1GFP (III) (from D. St. Johnston, Cambridge, UK and T. Uemura, respectively) and armadilloGal4 and UAS α-catenin GFP (II) [from Bloomington Stock Center and H. Oda (40), respectively] were used to label microtubule (plus ends) and cell junctions respectively, in all cells. No differences in any of the parameters measured were detected between Ubi DE-Cadherin GFP and armadillo Gal4 and UAS α-catenin GFP.…”

Section: Methodsmentioning

confidence: 99%

Integrin adhesion drives the emergent polarization of active cytoskeletal stresses to pattern cell delamination

Meghana

Ramdas

Hameed

et al. 2011

Proc. Natl. Acad. Sci. U.S.A.

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Tissue patterning relies on cellular reorganization through the interplay between signaling pathways and mechanical stresses. Their integration and spatiotemporal coordination remain poorly understood. Here we investigate the mechanisms driving the dynamics of cell delamination, diversely deployed to extrude dead cells or specify distinct cell fates. We show that a local mechanical stimulus (subcellular laser perturbation) releases cellular prestress and triggers cell delamination in the amnioserosa during Drosophila dorsal closure, which, like spontaneous delamination, results in the rearrangement of nearest neighbors around the delaminating cell into a rosette. We demonstrate that a sequence of "emergent cytoskeletal polarities" in the nearest neighbors (directed myosin flows, lamellipodial growth, polarized actomyosin collars, microtubule asters), triggered by the mechanical stimulus and dependent on integrin adhesion, generate active stresses that drive delamination. We interpret these patterns in the language of active gels as asters formed by active force dipoles involving surface and body stresses generated by each cell and liken delamination to mechanical yielding that ensues when these stresses exceed a threshold. We suggest that differential contributions of adhesion, cytoskeletal, and external stresses must underlie differences in spatial pattern.cell extrusion | cell mechanics | tissue dynamics | wound-healing T he establishment and maintenance of tissue pattern depends on cellular interactions mediated predominantly by the cadherin and integrin families of adhesion molecules. Their coupling to the (active) cytoskeleton enables mechanochemical transduction and through it the ability of cells in dynamic epithelia to actively generate, transmit, and sense mechanical stresses (1-4). How mechanochemical transduction is spatiotemporally regulated to facilitate the complex and diverse spatial patterns of tissues is poorly understood.The amnioserosa (AS) during dorsal closure in Drosophila provides a rich heterogeneity of patterned cell behaviors and an attractive in vivo model to address the interplay between adhesion, active forces, and cell behavior. Genetic and large-scale laser perturbations have shown that it is the principal driving force for dorsal closure (5-8). Its contraction by apical constriction [at ≈2 μm 2 /s during mid to late dorsal closure (5)] over the yolk cell helps establish continuity of the epidermis through the meeting of the leading edge cells of the epidermis to which it is bound (6,7,9). A small fraction of AS cells is also extruded seemingly stochastically from the epithelium (delamination) without compromising its integrity and is necessary for the timely completion of dorsal closure (9, 10). What underlies this stochasticity and how it is accommodated within the stereotypical dynamics of the AS remain unclear. Because delamination is commonly used to eliminate dead cells or to single out cells to adopt distinct fates, and is misregulated in cancers, an understanding of its pat...

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“…The following stocks were used: Canton S ('wildtype'); c381Gal4 ('AS::'; for amnioserosa expression; Bloomington Stock Center); armGal4 ('arm::'; for ubiquitous expression, from J.-P. Vincent, NIMR, London, UK); enGal4 ('en::'; for epidermal expression, e16E from A. H. Brand, Gurdon Institute, Cambridge, UK); Ubi DECadhGFP ('ECadhGFP'; from T. Uemura, Kyoto University, Japan) and UAS-cateninGFP [both to mark apical membranes (Oda and Tsukita, 1999)]; UAS-mitoGFP (to label mitochondria); UASactin5CGFP (to label expressing cells), both from Bloomington; and UAS-CD8::PARP-Venus [to detect 'caspase activity' (Williams et al, 2006)]. The following stocks were used to perturb the apoptotic cascade: UASrpr.C ('UAS-rpr', reaper overexpression), UAS-p35.H (UAS-p35) and hid 05014 ('hid' amorph), all from Bloomington Stock Center; UAS-hid [hid overexpression (Goyal et al, 2007)]; UAS-C ['UAS-ban'; bantam overexpression (Brennecke et al, 2003)]; UAS-DIAP1 (Hay and Guo, 2006); drp1 2 ['drp' mutant (Goyal et al, 2007) (Rikhy et al, 2007)].…”

Section: Drosophila Stocksmentioning

confidence: 99%

Spatial, temporal and molecular hierarchies in the link between death, delamination and dorsal closure

2011

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SUMMARYDead cells in most epithelia are eliminated by cell extrusion. Here, we explore whether cell delamination in the amnioserosa, a seemingly stochastic event that results in the extrusion of a small fraction of cells and known to provide a force for dorsal closure, is contingent upon the receipt of an apoptotic signal. Through the analysis of mutant combinations and the profiling of apoptotic signals in situ, we establish spatial, temporal and molecular hierarchies in the link between death and delamination. We show that although an apoptotic signal is necessary and sufficient to provide cell-autonomous instructions for delamination, its induction during natural delamination occurs downstream of mitochondrial fragmentation. We further show that apoptotic regulators can influence both delamination and dorsal closure cell non-autonomously, presumably by influencing tissue mechanics. The spatial heterogeneities in delamination frequency and mitochondrial morphology suggest that mechanical stresses may underlie the activation of the apoptotic cascade through their influence on mitochondrial dynamics. Our results document for the first time the temporal propagation of an apoptotic signal in the context of cell behaviours that accomplish morphogenesis during development. They highlight the importance of mitochondrial dynamics and tissue mechanics in its regulation. Together, they provide novel insights into how apoptotic signals can be deployed to pattern tissues.

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Dynamic features of adherens junctions during Drosophila embryonic epithelial morphogenesis revealed by a D α-catenin-GFP fusion protein

Cited by 66 publications

References 19 publications

Fibroblast growth factor signalling controls successive cell behaviours during mesoderm layer formation in Drosophila

Fibroblast growth factor signalling controls successive cell behaviours during mesoderm layer formation in Drosophila

Integrin adhesion drives the emergent polarization of active cytoskeletal stresses to pattern cell delamination

Spatial, temporal and molecular hierarchies in the link between death, delamination and dorsal closure

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