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      The role and regulation of blebs in cell migration

      review-article
      1 , 3 , 2
      Current Opinion in Cell Biology
      Elsevier

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          Abstract

          Blebs are cellular protrusions that have been shown to be instrumental for cell migration in development and disease. Bleb expansion is driven by hydrostatic pressure generated in the cytoplasm by the contractile actomyosin cortex. The mechanisms of bleb formation thus fundamentally differ from the actin polymerization-based mechanisms responsible for lamellipodia expansion. In this review, we summarize recent findings relevant for the mechanics of bleb formation and the underlying molecular pathways. We then review the processes involved in determining the type of protrusion formed by migrating cells, in particular in vivo, in the context of embryonic development. Finally, we discuss how cells utilize blebs for their forward movement in the presence or absence of strong substrate attachment.

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          Plasticity of cell migration: a multiscale tuning model

          Cell migration underlies tissue formation, maintenance, and regeneration as well as pathological conditions such as cancer invasion. Structural and molecular determinants of both tissue environment and cell behavior define whether cells migrate individually (through amoeboid or mesenchymal modes) or collectively. Using a multiparameter tuning model, we describe how dimension, density, stiffness, and orientation of the extracellular matrix together with cell determinants—including cell–cell and cell–matrix adhesion, cytoskeletal polarity and stiffness, and pericellular proteolysis—interdependently control migration mode and efficiency. Motile cells integrate variable inputs to adjust interactions among themselves and with the matrix to dictate the migration mode. The tuning model provides a matrix of parameters that control cell movement as an adaptive and interconvertible process with relevance to different physiological and pathological contexts.
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            Life at the leading edge.

            Cell migration requires sustained forward movement of the plasma membrane at the cell's front or "leading edge." To date, researchers have uncovered four distinct ways of extending the membrane at the leading edge. In lamellipodia and filopodia, actin polymerization directly pushes the plasma membrane forward, whereas in invadopodia, actin polymerization couples with the extracellular delivery of matrix-degrading metalloproteases to clear a path for cells through the extracellular matrix. Membrane blebs drive the plasma membrane forward using a combination of actomyosin-based contractility and reversible detachment of the membrane from the cortical actin cytoskeleton. Each protrusion type requires the coordination of a wide spectrum of signaling molecules and regulators of cytoskeletal dynamics. In addition, these different protrusion methods likely act in concert to move cells through complex environments in vivo. Copyright © 2011 Elsevier Inc. All rights reserved.
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              Rapid leukocyte migration by integrin-independent flowing and squeezing.

              All metazoan cells carry transmembrane receptors of the integrin family, which couple the contractile force of the actomyosin cytoskeleton to the extracellular environment. In agreement with this principle, rapidly migrating leukocytes use integrin-mediated adhesion when moving over two-dimensional surfaces. As migration on two-dimensional substrates naturally overemphasizes the role of adhesion, the contribution of integrins during three-dimensional movement of leukocytes within tissues has remained controversial. We studied the interplay between adhesive, contractile and protrusive forces during interstitial leukocyte chemotaxis in vivo and in vitro. We ablated all integrin heterodimers from murine leukocytes, and show here that functional integrins do not contribute to migration in three-dimensional environments. Instead, these cells migrate by the sole force of actin-network expansion, which promotes protrusive flowing of the leading edge. Myosin II-dependent contraction is only required on passage through narrow gaps, where a squeezing contraction of the trailing edge propels the rigid nucleus.
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                Author and article information

                Contributors
                Journal
                Curr Opin Cell Biol
                Curr. Opin. Cell Biol
                Current Opinion in Cell Biology
                Elsevier
                0955-0674
                1879-0410
                1 October 2013
                October 2013
                : 25
                : 5
                : 582-590
                Affiliations
                [1 ]Medical Research Council, Laboratory for Molecular Cell Biology, University College London, Gower Street, WC1E 6BT London, UK
                [2 ]Institute for Cell Biology, Center of Molecular Biology of Inflammation, University of Münster, Von-Esmarch-Strasse 56, Münster, Germany
                [3 ]International Institute of Molecular Cell Biology, Warsaw, Poland
                Article
                S0955-0674(13)00079-3
                10.1016/j.ceb.2013.05.005
                3989058
                23786923
                09a64ff1-cb2e-4a7d-aa72-137511783d09
                © 2013 Elsevier Ltd.

                This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/3.0/).

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                Cell biology
                Cell biology

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