A contractile actomyosin network linked to adherens junctions by Canoe/afadin helps drive convergent extension

Sawyer, Jessica K.; Choi, Wangsun; Jung, Kuo Chen; He, Li; Harris, Nathan; Peifer, Mark

doi:10.1091/mbc.e11-05-0411

Cited by 161 publications

(269 citation statements)

References 39 publications

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“…Recent work has demonstrated that this separate, apically localized pool of pulsating myosin-II is connected to AJs. Whereas this apical myosin-II clearly contributes to body elongation, it seems dispensable for rosette formation; in mutants in which apical myosin-II is specifically disrupted, rosettes still form, although apical myosin-II forms rings around vertices instead of its usual tight localization around rosette centers (Sawyer et al, 2011). Thus, myosin-II-dependent rosette formation and resolution is just one of at least two myosin-dependent mechanisms that lead to epithelial tissue elongation.…”

Section: Drosophila Epithelial Morphogenesismentioning

confidence: 99%

The roles and regulation of multicellular rosette structures during morphogenesis

2014

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Multicellular rosettes have recently been appreciated as important cellular intermediates that are observed during the formation of diverse organ systems. These rosettes are polarized, transient epithelial structures that sometimes recapitulate the form of the adult organ. Rosette formation has been studied in various developmental contexts, such as in the zebrafish lateral line primordium, the vertebrate pancreas, the Drosophila epithelium and retina, as well as in the adult neural stem cell niche. These studies have revealed that the cytoskeletal rearrangements responsible for rosette formation appear to be conserved. By contrast, the extracellular cues that trigger these rearrangements in vivo are less well understood and are more diverse. Here, we review recent studies of the genetic regulation and cellular transitions involved in rosette formation. We discuss and compare specific models for rosette formation and highlight outstanding questions in the field.

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Section: Drosophila Epithelial Morphogenesismentioning

confidence: 99%

The roles and regulation of multicellular rosette structures during morphogenesis

2014

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“…Considering that (i) drebrin may influence myosin activity (Ishikawa et al, 2007;Kubota et al, 2010) and (ii) actomyosin contractility can be involved in the regulation of cell-cell contacts (Sawyer et al, 2011;Taguchi et al, 2011), we explored the potential role of the actomyosin system in drebrin-dependent regulation of cell junctions, using myosin II-inhibiting drugs such as Y-27632 (inhibiting ROCK) and blebbistatin (not shown). However, using a wide variety of conditions, we did not detect a significant influence on drebrin-dependent stability of nectin at junctions.…”

Section: (D-o) Confocal Images Of Huvec Expressing Mito-drebrin-pp-gfmentioning

confidence: 99%

Drebrin preserves endothelial integrity by stabilizing nectin at adherens junctions

Rehm

Panzer

Vliet

et al. 2013

Journal of Cell Science

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SummaryRegulation of cell-cell contacts is essential for integrity of the vascular endothelium. Here, a critical role of the F-actin-binding protein drebrin in maintaining endothelial integrity is revealed under conditions mimicking vascular flow. Drebrin knockdown leads to weakening of cell-cell contacts, characterized by loss of nectin from adherens junctions and its subsequent lysosomal degradation. Immunoprecipitation, FRAP and mitochondrial re-targeting experiments show that nectin stabilization occurs through a chain of interactions: drebrin binding to F-actin, interaction of drebrin and afadin through their polyproline and PR1-2 regions, and recruitment of nectin through the PDZ region of afadin. Key elements are modules in drebrin that confer binding to afadin and F-actin. Evidence for this was obtained using constructs containing the PDZ region of afadin coupled to the F-actin-binding region of drebrin or to lifeact, which restore junctional nectin under knockdown of drebrin or of both drebrin and afadin. Drebrin, containing binding sites for both afadin and Factin, is thus uniquely equipped to stabilize nectin at endothelial junctions and to preserve endothelial integrity under vascular flow.

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“…(C) Shear stress that is generated by the flow of body fluid acts on surfaces of tubular tissues formed by endothelial or epithelial layers, as experienced by endothelial cells in blood vessels (Vermot et al, 2009). (D) Hydrostatic pressure exerted by a non-compressible internal tissue on a shrinking outer epithelial tubule, as observed during C. elegans embryonic elongation (Ciarletta et al, 2009 junction shrinkage during Drosophila germband cell intercalation (Fernandez-Gonzalez and Zallen, 2011;Rauzi et al, 2010;Sawyer et al, 2011). In contrast to cells without overt tissue planar polarity (fly mesoderm and amnioserosa), germband cells are polarized.…”

Section: Generation Of Intrinsic Forces Within Cellsmentioning

confidence: 99%

“…Here, myosin II foci preferentially move towards junctions with less E-cadherin (Rauzi et al, 2010). This pulse is regulated by a-Catenin and Canoe, which promote interactions between actomyosin and adherens junctions (Rauzi et al, 2010;Sawyer et al, 2011). The primary cause for the pulsatile nature of actomyosin foci probably reflects the dynamic instability that was observed for ensembles of motor proteins under load (Jülicher and Prost, 1995;Kruse and Riveline, 2011).…”

Section: Generation Of Intrinsic Forces Within Cellsmentioning

confidence: 99%

Signalling through mechanical inputs – a coordinated process

Zhang

Labouesse

2012

Journal of Cell Science

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SummaryThere is growing awareness that mechanical forces -in parallel to electrical or chemical inputs -have a central role in driving development and influencing the outcome of many diseases. However, we still have an incomplete understanding of how such forces function in coordination with each other and with other signalling inputs in vivo. Mechanical forces, which are generated throughout the organism, can produce signals through force-sensitive processes. Here, we first explore the mechanisms through which forces can be generated and the cellular responses to forces by discussing several examples from animal development. We then go on to examine the mechanotransduction-induced signalling processes that have been identified in vivo. Finally, we discuss what is known about the specificity of the responses to different forces, the mechanisms that might stabilize cells in response to such forces, and the crosstalk between mechanical forces and chemical signalling. Where known, we mention kinetic parameters that characterize forces and their responses. The multi-layered regulatory control of force generation, force response and force adaptation should be viewed as a wellintegrated aspect in the greater biological signalling systems.

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A contractile actomyosin network linked to adherens junctions by Canoe/afadin helps drive convergent extension

Cited by 161 publications

References 39 publications

The roles and regulation of multicellular rosette structures during morphogenesis

The roles and regulation of multicellular rosette structures during morphogenesis

Drebrin preserves endothelial integrity by stabilizing nectin at adherens junctions

Signalling through mechanical inputs – a coordinated process

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