Anisotropies in cortical tension reveal the physical basis of polarizing cortical flows

Mayer, Mirjam; Depken, Martin; Bois, Justin S.; Jülicher, Frank; Grill, Stephan W.

doi:10.1038/nature09376

Cited by 448 publications

(576 citation statements)

References 46 publications

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“…Laser ablation was used to analyse in vivo the forces generated by actomyosin structures organized in apical layers or cables 29,37,38 . Only a few studies have focused on the cortical actomyosin mesh of rounded cells, but these were done in cultured cells or in vivo-isolated cells, and none were done in mitotic cells 26,39 . Here we used laser microsurgery to analyse the mechanics of mitotic rounding cells in the context of a vertebrate epithelium.…”

Section: Discussionmentioning

confidence: 99%

Mitotic cell rounding and epithelial thinning regulate lumen growth and shape

et al. 2015

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Many organ functions rely on epithelial cavities with particular shapes. Morphogenetic anomalies in these cavities lead to kidney, brain or inner ear diseases. Despite their relevance, the mechanisms regulating lumen dimensions are poorly understood. Here, we perform live imaging of zebrafish inner ear development and quantitatively analyse the dynamics of lumen growth in 3D. Using genetic, chemical and mechanical interferences, we identify two new morphogenetic mechanisms underlying anisotropic lumen growth. The first mechanism involves thinning of the epithelium as the cells change their shape and lose fluids in concert with expansion of the cavity, suggesting an intra-organ fluid redistribution process. In the second mechanism, revealed by laser microsurgery experiments, mitotic rounding cells apicobasally contract the epithelium and mechanically contribute to expansion of the lumen. Since these mechanisms are axis specific, they not only regulate lumen growth but also the shape of the cavity.

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Section: Discussionmentioning

confidence: 99%

Mitotic cell rounding and epithelial thinning regulate lumen growth and shape

et al. 2015

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“…If we assume that dissipation of this force occurs between AS cells at these timescales (23), η =1 Pa s (24) and d ≈100 nm (25), then the distribution of slopes from this initial expansion phase gives a narrow distribution of prestress, typically on the order of 12-15 N m −2 ( Fig. 1E′) and at the lower end of the range of magnitudes reported elsewhere (26).…”

Section: Subcellular Cytoplasmic Laser Perturbation Releases Prestresmentioning

confidence: 94%

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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“…To measure cortical tension, we used laser nanoablation 19 to cut the cortical actin network. We then measured the instantaneous rate of recoil as an index of cortical actin network tension 30 . These laser nanoablation experiments were performed on cells that were untreated (control), preincubated with blebbistatin or stimulated with Ba 2 þ .…”

Section: Svs and Cortical Actin Approach The Plasmalemma On Stimulationmentioning

confidence: 99%

Activity-driven relaxation of the cortical actomyosin II network synchronizes Munc18-1-dependent neurosecretory vesicle docking

et al. 2015

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In neurosecretory cells, secretory vesicles (SVs) undergo Ca 2 þ -dependent fusion with the plasma membrane to release neurotransmitters. How SVs cross the dense mesh of the cortical actin network to reach the plasma membrane remains unclear. Here we reveal that, in bovine chromaffin cells, SVs embedded in the cortical actin network undergo a highly synchronized transition towards the plasma membrane and Munc18-1-dependent docking in response to secretagogues. This movement coincides with a translocation of the cortical actin network in the same direction. Both effects are abolished by the knockdown or the pharmacological inhibition of myosin II, suggesting changes in actomyosin-generated forces across the cell cortex. Indeed, we report a reduction in cortical actin network tension elicited on secretagogue stimulation that is sensitive to myosin II inhibition. We reveal that the cortical actin network acts as a 'casting net' that undergoes activity-dependent relaxation, thereby driving tethered SVs towards the plasma membrane where they undergo Munc18-1-dependent docking.

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Anisotropies in cortical tension reveal the physical basis of polarizing cortical flows

Cited by 448 publications

References 46 publications

Mitotic cell rounding and epithelial thinning regulate lumen growth and shape

Mitotic cell rounding and epithelial thinning regulate lumen growth and shape

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

Activity-driven relaxation of the cortical actomyosin II network synchronizes Munc18-1-dependent neurosecretory vesicle docking

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