Статті в журналах: "Actin Waves"

1

Wu, Min. "Deconstructing Actin Waves." Structure 27, no. 8 (August 2019): 1187–89. http://dx.doi.org/10.1016/j.str.2019.07.010.

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2

Iuliano, Olga, Azumi Yoshimura, Marie-Thérèse Prospéri, René Martin, Hans-Joachim Knölker, and Evelyne Coudrier. "Myosin 1b promotes axon formation by regulating actin wave propagation and growth cone dynamics." Journal of Cell Biology 217, no. 6 (March 27, 2018): 2033–46. http://dx.doi.org/10.1083/jcb.201703205.

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Single-headed myosin 1 has been identified in neurons, but its function in these cells is still unclear. We demonstrate that depletion of myosin 1b (Myo1b), inhibition of its motor activity, or its binding to phosphoinositides impairs the formation of the axon, whereas overexpression of Myo1b increases the number of axon-like structures. Myo1b is associated with growth cones and actin waves, two major contributors to neuronal symmetry breaking. We show that Myo1b controls the dynamics of the growth cones and the anterograde propagation of the actin waves. By coupling the membrane to the actin cytoskeleton, Myo1b regulates the size of the actin network as well as the stability and size of filopodia in the growth cones. Our data provide the first evidence that a myosin 1 plays a major role in neuronal symmetry breaking and argue for a mechanical control of the actin cytoskeleton both in actin waves and in the growth cones by this myosin.

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3

Mortal, Simone, Federico Iseppon, Andrea Perissinotto, Elisa D'Este, Dan Cojoc, Luisa M. R. Napolitano, and Vincent Torre. "Functions and Dynamics of Actin Waves." Biophysical Journal 114, no. 3 (February 2018): 142a. http://dx.doi.org/10.1016/j.bpj.2017.11.798.

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4

Beta, Carsten, Nir S. Gov, and Arik Yochelis. "Why a Large-Scale Mode Can Be Essential for Understanding Intracellular Actin Waves." Cells 9, no. 6 (June 23, 2020): 1533. http://dx.doi.org/10.3390/cells9061533.

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During the last decade, intracellular actin waves have attracted much attention due to their essential role in various cellular functions, ranging from motility to cytokinesis. Experimental methods have advanced significantly and can capture the dynamics of actin waves over a large range of spatio-temporal scales. However, the corresponding coarse-grained theory mostly avoids the full complexity of this multi-scale phenomenon. In this perspective, we focus on a minimal continuum model of activator–inhibitor type and highlight the qualitative role of mass conservation, which is typically overlooked. Specifically, our interest is to connect between the mathematical mechanisms of pattern formation in the presence of a large-scale mode, due to mass conservation, and distinct behaviors of actin waves.

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5

Krueger, Eugene W., James D. Orth, Hong Cao, and Mark A. McNiven. "A Dynamin–Cortactin–Arp2/3 Complex Mediates Actin Reorganization in Growth Factor-stimulated Cells." Molecular Biology of the Cell 14, no. 3 (March 2003): 1085–96. http://dx.doi.org/10.1091/mbc.e02-08-0466.

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The mechanisms by which mammalian cells remodel the actin cytoskeleton in response to motogenic stimuli are complex and a topic of intense study. Dynamin 2 (Dyn2) is a large GTPase that interacts directly with several actin binding proteins, including cortactin. In this study, we demonstrate that Dyn2 and cortactin function to mediate dynamic remodeling of the actin cytoskeleton in response to stimulation with the motogenic growth factor platelet-derived growth factor. On stimulation, Dyn2 and cortactin coassemble into large, circular structures on the dorsal cell surface. These “waves” promote an active reorganization of actin filaments in the anterior cytoplasm and function to disassemble actin stress fibers. Importantly, inhibition of Dyn2 and cortactin function potently blocked the formation of waves and subsequent actin reorganization. These findings demonstrate that cortactin and Dyn2 function together in a supramolecular complex that assembles in response to growth factor stimulation and mediates the remodeling of actin to facilitate lamellipodial protrusion at the leading edge of migrating cells.

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6

Masters, Thomas A., Michael P. Sheetz, and Nils C. Gauthier. "F-actin waves, actin cortex disassembly and focal exocytosis driven by actin-phosphoinositide positive feedback." Cytoskeleton 73, no. 4 (April 2016): 180–96. http://dx.doi.org/10.1002/cm.21287.

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7

Brembu, Tore, Per Winge, and Atle M. Bones. "Catching the WAVEs of Plant Actin Regulation." Journal of Plant Growth Regulation 24, no. 2 (June 2005): 55–66. http://dx.doi.org/10.1007/s00344-005-1013-y.

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8

Asano, Yukako, Akira Nagasaki, and Taro Q. P. Uyeda. "Correlated waves of actin filaments and PIP3inDictyosteliumcells." Cell Motility and the Cytoskeleton 65, no. 12 (December 2008): 923–34. http://dx.doi.org/10.1002/cm.20314.

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9

Ecke, Mary, Jana Prassler, Patrick Tanribil, Annette Müller-Taubenberger, Sarah Körber, Jan Faix, and Günther Gerisch. "Formins specify membrane patterns generated by propagating actin waves." Molecular Biology of the Cell 31, no. 5 (March 1, 2020): 373–85. http://dx.doi.org/10.1091/mbc.e19-08-0460.

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Actin waves beneath the membrane of Dictyostelium cells separate two distinct areas of the cell cortex. Upon wave propagation, one type of area is converted into the other. We show that specific formins are recruited to different areas of the wave landscape and use these actin-polymerizing machines to analyze the dynamics of pattern formation.

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10

Gerisch, Günther, Till Bretschneider, Annette Müller-Taubenberger, Evelyn Simmeth, Mary Ecke, Stefan Diez, and Kurt Anderson. "Mobile Actin Clusters and Traveling Waves in Cells Recovering from Actin Depolymerization." Biophysical Journal 87, no. 5 (November 2004): 3493–503. http://dx.doi.org/10.1529/biophysj.104.047589.

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11

Zhang, Ke, Wanqing Lyu, Ji Yu, and Anthony J. Koleske. "Abl2 is recruited to ventral actin waves through cytoskeletal interactions to promote lamellipodium extension." Molecular Biology of the Cell 29, no. 23 (November 15, 2018): 2863–73. http://dx.doi.org/10.1091/mbc.e18-01-0044.

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Abl family nonreceptor tyrosine kinases regulate changes in cell shape and migration. Abl2 localizes to dynamic actin-rich protrusions, such as lamellipodia in fibroblasts and dendritic spines in neurons. Abl2 interactions with cortactin, an actin filament stabilizer, are crucial for the formation and stability of actin-rich structures, but Abl2:cortactin-positive structures have not been characterized with high spatiotemporal resolution in cells. Using total internal reflection fluorescence microscopy, we demonstrate that Abl2 colocalizes with cortactin at wave-like structures within lamellum and lamellipodium tips. Abl2 and cortactin within waves are focal and transient, extend to the outer edge of lamella, and serve as the base for lamellipodia protrusions. Abl2-positive foci colocalize with integrin β3 and paxillin, adhesive markers of the lamellum–lamellipodium interface. Cortactin-positive waves still form in Abl2 knockout cells, but the lamellipodium size is significantly reduced. This deficiency is restored following Abl2 reexpression. Complementation analyses revealed that the Abl2 C-terminal half, which contains domains that bind actin and microtubules, is necessary and sufficient for recruitment to the wave-like structures and to support normal lamellipodium size, while the kinase domain–containing N-terminal half does not impact lamellipodium size. Together, this work demonstrates that Abl2 is recruited with cortactin to actin waves through cytoskeletal interactions to promote lamellipodium extension.

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12

Naoz, Moshe, and Nir S. Gov. "Cell-Substrate Patterns Driven by Curvature-Sensitive Actin Polymerization: Waves and Podosomes." Cells 9, no. 3 (March 23, 2020): 782. http://dx.doi.org/10.3390/cells9030782.

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Cells adhered to an external solid substrate are observed to exhibit rich dynamics of actin structures on the basal membrane, which are distinct from those observed on the dorsal (free) membrane. Here we explore the dynamics of curved membrane proteins, or protein complexes, that recruit actin polymerization when the membrane is confined by the solid substrate. Such curved proteins can induce the spontaneous formation of membrane protrusions on the dorsal side of cells. However, on the basal side of the cells, such protrusions can only extend as far as the solid substrate and this constraint can convert such protrusions into propagating wave-like structures. We also demonstrate that adhesion molecules can stabilize localized protrusions that resemble some features of podosomes. This coupling of curvature and actin forces may underlie the differences in the observed actin-membrane dynamics between the basal and dorsal sides of adhered cells.

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13

Gholami, Azam, Mihaela Enculescu, and Martin Falcke. "Membrane waves driven by forces from actin filaments." New Journal of Physics 14, no. 11 (November 2, 2012): 115002. http://dx.doi.org/10.1088/1367-2630/14/11/115002.

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14

Inagaki, Naoyuki, and Hiroko Katsuno. "Actin Waves: Origin of Cell Polarization and Migration?" Trends in Cell Biology 27, no. 7 (July 2017): 515–26. http://dx.doi.org/10.1016/j.tcb.2017.02.003.

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15

Veksler, Alex, and Nir S. Gov. "Calcium-Actin Waves and Oscillations of Cellular Membranes." Biophysical Journal 97, no. 6 (September 2009): 1558–68. http://dx.doi.org/10.1016/j.bpj.2009.07.008.

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16

Carlsson, Anders E. "Traveling Waves and Patches in Dendritic Actin Nucleation." Biophysical Journal 100, no. 3 (February 2011): 445a. http://dx.doi.org/10.1016/j.bpj.2010.12.2621.

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17

Giannone, Grégory, Benjamin J. Dubin-Thaler, Hans-Günther Döbereiner, Nelly Kieffer, Anne R. Bresnick, and Michael P. Sheetz. "Periodic Lamellipodial Contractions Correlate with Rearward Actin Waves." Cell 116, no. 3 (February 2004): 431–43. http://dx.doi.org/10.1016/s0092-8674(04)00058-3.

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18

Allard, Jun, and Alex Mogilner. "Traveling waves in actin dynamics and cell motility." Current Opinion in Cell Biology 25, no. 1 (February 2013): 107–15. http://dx.doi.org/10.1016/j.ceb.2012.08.012.

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19

Ecker, Nicolas, and Karsten Kruse. "Excitable actin dynamics and amoeboid cell migration." PLOS ONE 16, no. 2 (February 1, 2021): e0246311. http://dx.doi.org/10.1371/journal.pone.0246311.

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Amoeboid cell migration is characterized by frequent changes of the direction of motion and resembles a persistent random walk on long time scales. Although it is well known that cell migration is typically driven by the actin cytoskeleton, the cause of this migratory behavior remains poorly understood. We analyze the spontaneous dynamics of actin assembly due to nucleation promoting factors, where actin filaments lead to an inactivation of these factors. We show that this system exhibits excitable dynamics and can spontaneously generate waves, which we analyze in detail. By using a phase-field approach, we show that these waves can generate cellular random walks. We explore how the characteristics of these persistent random walks depend on the parameters governing the actin-nucleator dynamics. In particular, we find that the effective diffusion constant and the persistence time depend strongly on the speed of filament assembly and the rate of nucleator inactivation. Our findings point to a deterministic origin of the random walk behavior and suggest that cells could adapt their migration pattern by modifying the pool of available actin.

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20

Stankevicins, Luiza, Nicolas Ecker, Emmanuel Terriac, Paolo Maiuri, Rouven Schoppmeyer, Pablo Vargas, Ana-Maria Lennon-Duménil, et al. "Deterministic actin waves as generators of cell polarization cues." Proceedings of the National Academy of Sciences 117, no. 2 (December 27, 2019): 826–35. http://dx.doi.org/10.1073/pnas.1907845117.

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Dendritic cells “patrol” the human body to detect pathogens. In their search, dendritic cells perform a random walk by amoeboid migration. The efficiency of pathogen detection depends on the properties of the random walk. It is not known how the dendritic cells control these properties. Here, we quantify dendritic cell migration under well-defined 2-dimensional confinement and in a 3-dimensional collagen matrix through recording their long-term trajectories. We find 2 different migration states: persistent migration, during which the dendritic cells move along curved paths, and diffusive migration, which is characterized by successive sharp turns. These states exhibit differences in the actin distributions. Our theoretical and experimental analyses indicate that this kind of motion can be generated by spontaneous actin polymerization waves that contribute to dendritic cell polarization and migration. The relative distributions of persistent and diffusive migration can be changed by modification of the molecular actin filament nucleation and assembly rates. Thus, dendritic cells can control their migration patterns and adapt to specific environments. Our study offers an additional perspective on how dendritic cells tune their searches for pathogens.

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21

Haston, W. S. "F-actin distribution in polymorphonuclear leucocytes." Journal of Cell Science 88, no. 4 (November 1, 1987): 495–501. http://dx.doi.org/10.1242/jcs.88.4.495.

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The polarization and amoeboid locomotion of neutrophil leucocytes is stimulated by chemotactic factors, which initiate waves of contraction in both adherent and non-adherent neutrophils. These cyclical contractile events have previously been analysed by time-lapse filming but the mechanisms involved in the coordination of the cytoskeleton during locomotion have not been elucidated, one reason being because of the problems involved in fixing motile cells. In this paper we show that improved fixation of motile neutrophils with low concentrations of glutaraldehyde followed by glycine quenching demonstrated significant differences in the pattern of staining with TRITC-phalloidin in neutrophils moving on different substrata. Previous film analysis had shown the basic features of locomotion to be similar on all substrata. A prominent feature of leucocyte locomotion on two-dimensional substrata (e.g. protein-coated glass), on three-dimensional collagen gels or in motile cells floating in suspension, is the wave of contraction that passes antero-posteriorly along the length of the cell. The organization of the cytoskeletal elements has not been demonstrated at contraction waves, but light fixation with glutaraldehyde followed by staining with TRITC-phalloidin demonstrated prominent bands of F-actin in neutrophils inside collagen gels. These bands were not present in neutrophils either in suspension or moving on a two-dimensional substratum. Although all motile neutrophils had brightly stained anterior lamellipodia, the cells moving on the two-dimensional substratum had very extensively ruffled leading lamellae stained very brightly with TRITC-phalloidin. The reasons for the absence of consistent bands of F-actin at contraction waves are discussed.

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22

Guetta-Terrier, Charlotte, Pascale Monzo, Jie Zhu, Hongyan Long, Lakshmi Venkatraman, Yue Zhou, PeiPei Wang, et al. "Protrusive waves guide 3D cell migration along nanofibers." Journal of Cell Biology 211, no. 3 (November 9, 2015): 683–701. http://dx.doi.org/10.1083/jcb.201501106.

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In vivo, cells migrate on complex three-dimensional (3D) fibrous matrices, which has made investigation of the key molecular and physical mechanisms that drive cell migration difficult. Using reductionist approaches based on 3D electrospun fibers, we report for various cell types that single-cell migration along fibronectin-coated nanofibers is associated with lateral actin-based waves. These cyclical waves have a fin-like shape and propagate up to several hundred micrometers from the cell body, extending the leading edge and promoting highly persistent directional movement. Cells generate these waves through balanced activation of the Rac1/N-WASP/Arp2/3 and Rho/formins pathways. The waves originate from one major adhesion site at leading end of the cell body, which is linked through actomyosin contractility to another site at the back of the cell, allowing force generation, matrix deformation and cell translocation. By combining experimental and modeling data, we demonstrate that cell migration in a fibrous environment requires the formation and propagation of dynamic, actin based fin-like protrusions.

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23

Gerisch, Guenther, Mary Ecke, Britta Schroth-Diez, Silke Gerwig, Ulrike Engel, Lucinda Maddera, and Margaret Clarke. "Self-organizing actin waves as planar phagocytic cup structures." Cell Adhesion & Migration 3, no. 4 (October 2009): 373–82. http://dx.doi.org/10.4161/cam.3.4.9708.

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24

Khamviwath, Varunyu, Jifeng Hu, and Hans G. Othmer. "A Continuum Model of Actin Waves in Dictyostelium discoideum." PLoS ONE 8, no. 5 (May 31, 2013): e64272. http://dx.doi.org/10.1371/journal.pone.0064272.

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25

Dreher, A., I. S. Aranson, and K. Kruse. "Spiral actin-polymerization waves can generate amoeboidal cell crawling." New Journal of Physics 16, no. 5 (May 9, 2014): 055007. http://dx.doi.org/10.1088/1367-2630/16/5/055007.

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26

Roy, Subhojit. "Waves, rings, and trails: The scenic landscape of axonal actin." Journal of Cell Biology 212, no. 2 (January 11, 2016): 131–34. http://dx.doi.org/10.1083/jcb.201511016.

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The goal of this article is to provide the reader a snapshot of recent studies on axonal actin—largely emerging from superresolution and live-imaging experiments—and place this new information in context with earlier studies.

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27

Sirotkin, Vladimir, Julien Berro, Keely Macmillan, Lindsey Zhao, and Thomas D. Pollard. "Quantitative Analysis of the Mechanism of Endocytic Actin Patch Assembly and Disassembly in Fission Yeast." Molecular Biology of the Cell 21, no. 16 (August 15, 2010): 2894–904. http://dx.doi.org/10.1091/mbc.e10-02-0157.

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We used quantitative confocal microscopy to measure the numbers of 16 proteins tagged with fluorescent proteins during assembly and disassembly of endocytic actin patches in fission yeast. The peak numbers of each molecule that accumulate in patches varied <30–50% between individual patches. The pathway begins with accumulation of 30–40 clathrin molecules, sufficient to build a hemisphere at the tip of a plasma membrane invagination. Thereafter precisely timed waves of proteins reach characteristic peak numbers: endocytic adaptor proteins (∼120 End4p and ∼230 Pan1p), activators of Arp2/3 complex (∼200 Wsp1p and ∼340 Myo1p) and ∼300 Arp2/3 complexes just ahead of a burst of actin assembly into short, capped and highly cross-linked filaments (∼7000 actins, ∼200 capping proteins, and ∼900 fimbrins). Coronin arrives last as all other components disperse upon patch internalization and movement over ∼10 s. Patch internalization occurs without recruitment of dynamins. Mathematical modeling, described in the accompanying paper (Berro et al., 2010, MBoC 21: 2905–2915), shows that the dendritic nucleation hypothesis can account for the time course of actin assembly into a branched network of several hundred filaments 100–200 nm long and that patch disassembly requires actin filament fragmentation in addition to depolymerization from the ends.

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28

Case, Lindsay B., and Clare M. Waterman. "Adhesive F-actin Waves: A Novel Integrin-Mediated Adhesion Complex Coupled to Ventral Actin Polymerization." PLoS ONE 6, no. 11 (November 1, 2011): e26631. http://dx.doi.org/10.1371/journal.pone.0026631.

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29

Yamazaki, Shota, Yuya Ueno, Ryosuke Hosoki, Takanori Saito, Toshitaka Idehara, Yuusuke Yamaguchi, Chiko Otani, Yuichi Ogawa, Masahiko Harata, and Hiromichi Hoshina. "THz irradiation inhibits cell division by affecting actin dynamics." PLOS ONE 16, no. 8 (August 2, 2021): e0248381. http://dx.doi.org/10.1371/journal.pone.0248381.

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Biological phenomena induced by terahertz (THz) irradiation are described in recent reports, but underlying mechanisms, structural and dynamical change of specific molecules are still unclear. In this paper, we performed time-lapse morphological analysis of human cells and found that THz irradiation halts cell division at cytokinesis. At the end of cytokinesis, the contractile ring, which consists of filamentous actin (F-actin), needs to disappear; however, it remained for 1 hour under THz irradiation. Induction of the functional structures of F-actin was also observed in interphase cells. Similar phenomena were also observed under chemical treatment (jasplakinolide), indicating that THz irradiation assists actin polymerization. We previously reported that THz irradiation enhances the polymerization of purified actin in vitro; our current work shows that it increases cytoplasmic F-actin in vivo. Thus, we identified one of the key biomechanisms affected by THz waves.

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30

Boyer, Laurent, Anne Doye, Monica Rolando, Gilles Flatau, Patrick Munro, Pierre Gounon, René Clément, et al. "Induction of transient macroapertures in endothelial cells through RhoA inhibition by Staphylococcus aureus factors." Journal of Cell Biology 173, no. 5 (June 5, 2006): 809–19. http://dx.doi.org/10.1083/jcb.200509009.

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The GTPase RhoA is a major regulator of the assembly of actin stress fibers and the contractility of the actomyosin cytoskeleton. The epidermal cell differentiation inhibitor (EDIN) and EDIN-like ADP-ribosyltransferases of Staphylococcus aureus catalyze the inactivation of RhoA, producing actin cable disruption. We report that purified recombinant EDIN and EDIN-producing S. aureus provoke large transcellular tunnels in endothelial cells that we have named macroapertures (MAs). These structures open transiently, followed by the appearance of actin-containing membrane waves extending over the aperture. Disruption of actin cables, either directly or indirectly, through rhoA RNAi knockdown also triggers the formation of MAs. Intoxication of endothelial monolayers by EDIN produces a loss of barrier function and provides direct access of the endothelium basement membrane to S. aureus.

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31

Avila Ponce de León, Marco A., Bryan Félix, and Hans G. Othmer. "A phosphoinositide-based model of actin waves in frustrated phagocytosis." Journal of Theoretical Biology 527 (October 2021): 110764. http://dx.doi.org/10.1016/j.jtbi.2021.110764.

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32

Holmes, William R., and Leah Edelstein-Keshet. "A Biochemical Model for Sub-Cellular Waves of Actin Activity." Biophysical Journal 102, no. 3 (January 2012): 375a—376a. http://dx.doi.org/10.1016/j.bpj.2011.11.2051.

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33

Phillips, J. C. "Self-organized networks: Darwinian evolution of dynein rings, stalks, and stalk heads." Proceedings of the National Academy of Sciences 117, no. 14 (March 23, 2020): 7799–802. http://dx.doi.org/10.1073/pnas.1920840117.

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Cytoskeletons are self-organized networks based on polymerized proteins: actin, tubulin, and driven by motor proteins, such as myosin, kinesin, and dynein. Their positive Darwinian evolution enables them to approach optimized functionality (self-organized criticality). Dynein has three distinct titled subunits, but how these units connect to function as a molecular motor is mysterious. Dynein binds to tubulin through two coiled coil stalks and a stalk head. The energy used to alter the head binding and propel cargo along tubulin is supplied by ATP at a ring 1,500 amino acids away. Here, we show how many details of this extremely distant interaction are explained by water waves quantified by thermodynamic scaling. Water waves have shaped all proteins throughout positive Darwinian evolution, and many aspects of long-range water–protein interactions are universal (described by self-organized criticality). Dynein water waves resembling tsunami produce nearly optimal energy transport over 1,500 amino acids along dynein’s one-dimensional peptide backbone. More specifically, this paper identifies many similarities in the function and evolution of dynein compared to other cytoskeleton proteins such as actin, myosin, and tubulin.

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34

Brzeska, Hanna, Jesus Gonzalez, Edward D. Korn, and Margaret A. Titus. "Basic-hydrophobic sites are localized in conserved positions inside and outside of PH domains and affect localization of Dictyostelium myosin 1s." Molecular Biology of the Cell 31, no. 2 (January 15, 2020): 101–17. http://dx.doi.org/10.1091/mbc.e19-08-0475.

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Comparison of the highly dynamic localizations of Dictyostelium myosin 1s reveals significant differences between their localizations in macropinocytic protrusions and in actin waves. The short basic-hydrophobic sites lie in conserved positions and are the important determinants of myosin 1s localization.

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35

Fukujin, Fumihito, Akihiko Nakajima, Nao Shimada, and Satoshi Sawai. "Self-organization of chemoattractant waves in Dictyostelium depends on F-actin and cell–substrate adhesion." Journal of The Royal Society Interface 13, no. 119 (June 2016): 20160233. http://dx.doi.org/10.1098/rsif.2016.0233.

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In the social amoeba Dictyostelium discoideum , travelling waves of extracellular cyclic adenosine monophosphate (cAMP) self-organize in cell populations and direct aggregation of individual cells to form multicellular fruiting bodies. In contrast to the large body of studies that addressed how movement of cells is determined by spatial and temporal cues encoded in the dynamic cAMP gradients, how cell mechanics affect the formation of a self-generated chemoattractant field has received less attention. Here, we show, by live cell imaging analysis, that the periodicity of the synchronized cAMP waves increases in cells treated with the actin inhibitor latrunculin. Detail analysis of the extracellular cAMP-induced transients of cytosolic cAMP (cAMP relay response) in well-isolated cells demonstrated that their amplitude and duration were markedly reduced in latrunculin-treated cells. Similarly, in cells strongly adhered to a poly- l -lysine-coated surface, the response was suppressed, and the periodicity of the population-level oscillations was markedly lengthened. Our results suggest that cortical F-actin is dispensable for the basic low amplitude relay response but essential for its full amplification and that this enhanced response is necessary to establish high-frequency signalling centres. The observed F-actin dependence may prevent aggregation centres from establishing in microenvironments that are incompatible with cell migration.

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36

Antunes, Marco, Telmo Pereira, João V. Cordeiro, Luis Almeida, and Antonio Jacinto. "Coordinated waves of actomyosin flow and apical cell constriction immediately after wounding." Journal of Cell Biology 202, no. 2 (July 22, 2013): 365–79. http://dx.doi.org/10.1083/jcb.201211039.

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Epithelial wound healing relies on tissue movements and cell shape changes. Our work shows that, immediately after wounding, there was a dramatic cytoskeleton remodeling consisting of a pulse of actomyosin filaments that assembled in cells around the wound edge and flowed from cell to cell toward the margin of the wound. We show that this actomyosin flow was regulated by Diaphanous and ROCK and that it elicited a wave of apical cell constriction that culminated in the formation of the leading edge actomyosin cable, a structure that is essential for wound closure. Calcium signaling played an important role in this process, as its intracellular concentration increased dramatically immediately after wounding, and down-regulation of transient receptor potential channel M, a stress-activated calcium channel, also impaired the actomyosin flow. Lowering the activity of Gelsolin, a known calcium-activated actin filament–severing protein, also impaired the wound response, indicating that cleaving the existing actin filament network is an important part of the cytoskeleton remodeling process.

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37

Ibarra, N., A. Pollitt, and R. H. Insall. "Regulation of actin assembly by SCAR/WAVE proteins." Biochemical Society Transactions 33, no. 6 (October 26, 2005): 1243–46. http://dx.doi.org/10.1042/bst0331243.

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Actin reorganization is a tightly regulated process that co-ordinates complex cellular events, such as cell migration, chemotaxis, phagocytosis and adhesion, but the molecular mechanisms that underlie these processes are not well understood. SCAR (suppressor of cAMP receptor)/WAVE [WASP (Wiskott–Aldrich syndrome protein)-family verprolin homology protein] proteins are members of the conserved WASP family of cytoskeletal regulators, which play a critical role in actin dynamics by triggering Arp2/3 (actin-related protein 2/3)-dependent actin nucleation. SCAR/WAVEs are thought to be regulated by a pentameric complex which also contains Abi (Abl-interactor), Nap (Nck-associated protein), PIR121 (p53-inducible mRNA 121) and HSPC300 (haematopoietic stem progenitor cell 300), but the structural organization of the complex and the contribution of its individual components to the regulation of SCAR/WAVE function remain unclear. Additional features of SCAR/WAVE regulation are highlighted by the discovery of other interactors and distinct complexes. It is likely that the combinatorial assembly of different components of SCAR/WAVE complexes will prove to be vital for their roles at the centre of dynamic actin reorganization.

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38

Bohdanowicz, Michal, Gabriela Cosío, Jonathan M. Backer, and Sergio Grinstein. "Class I and class III phosphoinositide 3-kinases are required for actin polymerization that propels phagosomes." Journal of Cell Biology 191, no. 5 (November 29, 2010): 999–1012. http://dx.doi.org/10.1083/jcb.201004005.

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Actin polymerization drives the extension of pseudopods that trap and engulf phagocytic targets. The polymerized actin subsequently dissociates as the phagocytic vacuole seals and detaches from the plasma membrane. We found that phagosomes formed by engagement of integrins that serve as complement receptors (CR3) undergo secondary waves of actin polymerization, leading to the formation of “comet tails” that propel the vacuoles inside the cells. Actin tail formation was accompanied by and required de novo formation of PI(3,4)P2 and PI(3,4,5)P3 on the phagosomal membrane by class I phosphoinositide 3-kinases (PI3Ks). Although the phosphatidylinositide phosphatase Inpp5B was recruited to nascent phagosomes, it rapidly detached from the membrane after phagosomes sealed. Detachment of Inpp5B required the formation of PI(3)P. Thus, class III PI3K activity was also required for the accumulation of PI(4,5)P2 and PI(3,4,5)P3 and for actin tail formation. These experiments reveal a new PI(3)P-sensitive pathway leading to PI(3,4)P2 and PI(3,4,5)P3 formation and signaling in endomembranes.

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39

Sun, Xiaoyu, Meghan K. Driscoll, Can Guven, Satarupa Das, Carole A. Parent, John T. Fourkas, and Wolfgang Losert. "Asymmetric nanotopography biases cytoskeletal dynamics and promotes unidirectional cell guidance." Proceedings of the National Academy of Sciences 112, no. 41 (September 28, 2015): 12557–62. http://dx.doi.org/10.1073/pnas.1502970112.

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Many biological and physiological processes depend upon directed migration of cells, which is typically mediated by chemical or physical gradients or by signal relay. Here we show that cells can be guided in a single preferred direction based solely on local asymmetries in nano/microtopography on subcellular scales. These asymmetries can be repeated, and thereby provide directional guidance, over arbitrarily large areas. The direction and strength of the guidance is sensitive to the details of the nano/microtopography, suggesting that this phenomenon plays a context-dependent role in vivo. We demonstrate that appropriate asymmetric nano/microtopography can unidirectionally bias internal actin polymerization waves and that cells move with the same preferred direction as these waves. This phenomenon is observed both for the pseudopod-dominated migration of the amoeboid Dictyostelium discoideum and for the lamellipod-driven migration of human neutrophils. The conservation of this mechanism across cell types and the asymmetric shape of many natural scaffolds suggest that actin-wave-based guidance is important in biology and physiology.

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40

Wu, Min, Xudong Wu, and Pietro De Camilli. "Calcium oscillations-coupled conversion of actin travelling waves to standing oscillations." Proceedings of the National Academy of Sciences 110, no. 4 (January 7, 2013): 1339–44. http://dx.doi.org/10.1073/pnas.1221538110.

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41

Oelz, Dietmar, and Alex Mogilner. "Actomyosin contraction, aggregation and traveling waves in a treadmilling actin array." Physica D: Nonlinear Phenomena 318-319 (April 2016): 70–83. http://dx.doi.org/10.1016/j.physd.2015.10.005.

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42

Jasnin, Marion, Florian Beck, Mary Ecke, Yoshiyuki Fukuda, Antonio Martinez-Sanchez, Wolfgang Baumeister, and Günther Gerisch. "The Architecture of Traveling Actin Waves Revealed by Cryo-Electron Tomography." Structure 27, no. 8 (August 2019): 1211–23. http://dx.doi.org/10.1016/j.str.2019.05.009.

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43

Schroth‐Diez, Britta, Silke Gerwig, Mary Ecke, Reiner Hegerl, Stefan Diez, and Günther Gerisch. "Propagating waves separate two states of actin organization in living cells." HFSP Journal 3, no. 6 (December 2009): 412–27. http://dx.doi.org/10.2976/1.3239407.

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44

Peleg, Barak, Andrea Disanza, Giorgio Scita, and Nir Gov. "Propagating Cell-Membrane Waves Driven by Curved Activators of Actin Polymerization." PLoS ONE 6, no. 4 (April 21, 2011): e18635. http://dx.doi.org/10.1371/journal.pone.0018635.

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45

Woo, Doyeon, Yeji Seo, Hyunjin Jung, Sungsoo Kim, Nury Kim, Sang-Min Park, Heeyoung Lee, Sangkyu Lee, Kwang-Hyun Cho, and Won Do Heo. "Locally Activating TrkB Receptor Generates Actin Waves and Specifies Axonal Fate." Cell Chemical Biology 26, no. 12 (December 2019): 1652–63. http://dx.doi.org/10.1016/j.chembiol.2019.10.006.

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46

Brzeska, Hanna, Hilary Koech, Kevin J. Pridham, Edward D. Korn, and Margaret A. Titus. "Selective localization of myosin-I proteins in macropinosomes and actin waves." Cytoskeleton 73, no. 2 (February 2016): 68–82. http://dx.doi.org/10.1002/cm.21275.

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47

Noegel, Angelika A., Rosemarie Blau-Wasser, Hameeda Sultana, Rolf Müller, Lars Israel, Michael Schleicher, Hitesh Patel, and Cornelis J. Weijer. "The Cyclase-associated Protein CAP as Regulator of Cell Polarity and cAMP Signaling in Dictyostelium." Molecular Biology of the Cell 15, no. 2 (February 2004): 934–45. http://dx.doi.org/10.1091/mbc.e03-05-0269.

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Cyclase-associated protein (CAP) is an evolutionarily conserved regulator of the G-actin/F-actin ratio and, in yeast, is involved in regulating the adenylyl cyclase activity. We show that cell polarization, F-actin organization, and phototaxis are altered in a Dictyostelium CAP knockout mutant. Furthermore, in complementation assays we determined the roles of the individual domains in signaling and regulation of the actin cytoskeleton. We studied in detail the adenylyl cyclase activity and found that the mutant cells have normal levels of the aggregation phase-specific adenylyl cyclase and that receptor-mediated activation is intact. However, cAMP relay that is responsible for the generation of propagating cAMP waves that control the chemotactic aggregation of starving Dictyostelium cells was altered, and the cAMP-induced cGMP production was significantly reduced. The data suggest an interaction of CAP with adenylyl cyclase in Dictyostelium and an influence on signaling pathways directly as well as through its function as a regulatory component of the cytoskeleton.

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48

Sens, Pierre. "Stick–slip model for actin-driven cell protrusions, cell polarization, and crawling." Proceedings of the National Academy of Sciences 117, no. 40 (September 21, 2020): 24670–78. http://dx.doi.org/10.1073/pnas.2011785117.

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Cell crawling requires the generation of intracellular forces by the cytoskeleton and their transmission to an extracellular substrate through specific adhesion molecules. Crawling cells show many features of excitable systems, such as spontaneous symmetry breaking and crawling in the absence of external cues, and periodic and propagating waves of activity. Mechanical instabilities in the active cytoskeleton network and feedback loops in the biochemical network of activators and repressors of cytoskeleton dynamics have been invoked to explain these dynamical features. Here, I show that the interplay between the dynamics of cell–substrate adhesion and linear cellular mechanics is sufficient to reproduce many nonlinear dynamical patterns observed in spreading and crawling cells. Using an analytical formalism of the molecular clutch model of cell adhesion, regulated by local mechanical forces, I show that cellular traction forces exhibit stick–slip dynamics resulting in periodic waves of protrusion/retraction and propagating waves along the cell edge. This can explain spontaneous symmetry breaking and polarization of spreading cells, leading to steady crawling or bipedal motion, and bistability, where persistent cell motion requires a sufficiently strong transient external stimulus. The model also highlights the role of membrane tension in providing the long-range mechanical communication across the cell required for symmetry breaking.

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49

Wang, Chenlu, Sagar Chowdhury, Meghan Driscoll, Carole A. Parent, S. K. Gupta, and Wolfgang Losert. "The interplay of cell–cell and cell–substrate adhesion in collective cell migration." Journal of The Royal Society Interface 11, no. 100 (November 6, 2014): 20140684. http://dx.doi.org/10.1098/rsif.2014.0684.

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Collective cell migration often involves notable cell–cell and cell–substrate adhesions and highly coordinated motion of touching cells. We focus on the interplay between cell–substrate adhesion and cell–cell adhesion. We show that the loss of cell-surface contact does not significantly alter the dynamic pattern of protrusions and retractions of fast migrating amoeboid cells ( Dictyostelium discoideum ), but significantly changes their ability to adhere to other cells. Analysis of the dynamics of cell shapes reveals that cells that are adherent to a surface may coordinate their motion with neighbouring cells through protrusion waves that travel across cell–cell contacts. However, while shape waves exist if cells are detached from surfaces, they do not couple cell to cell. In addition, our investigation of actin polymerization indicates that loss of cell-surface adhesion changes actin polymerization at cell–cell contacts. To further investigate cell–cell/cell–substrate interactions, we used optical micromanipulation to form cell–substrate contact at controlled locations. We find that both cell-shape dynamics and cytoskeletal activity respond rapidly to the formation of cell–substrate contact.

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50

Shin, Dong Min, Xiao-Song Zhao, Weizhong Zeng, Marina Mozhayeva, and Shmuel Muallem. "The Mammalian Sec6/8 Complex Interacts with Ca2+ Signaling Complexes and Regulates Their Activity." Journal of Cell Biology 150, no. 5 (September 4, 2000): 1101–12. http://dx.doi.org/10.1083/jcb.150.5.1101.

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The localization of various Ca2+ transport and signaling proteins in secretory cells is highly restricted, resulting in polarized agonist-stimulated Ca2+ waves. In the present work, we examined the possible roles of the Sec6/8 complex or the exocyst in polarized Ca2+ signaling in pancreatic acinar cells. Immunolocalization by confocal microscopy showed that the Sec6/8 complex is excluded from tight junctions and secretory granules in these cells. The Sec6/8 complex was found in at least two cellular compartments, part of the complex showed similar, but not identical, localization with the Golgi apparatus and part of the complex associated with Ca2+ signaling proteins next to the plasma membrane at the apical pole. Accordingly, immunoprecipitation (IP) of Sec8 did not coimmunoprecipitate βCOP, Golgi 58K protein, or mannosidase II, all Golgi-resident proteins. By contrast, IP of Sec8 coimmunoprecipitates Sec6, type 3 inositol 1,4,5-trisphosphate receptors (IP3R3), and the Gβγ subunit of G proteins from pancreatic acinar cell extracts. Furthermore, the anti-Sec8 antibodies coimmunoprecipitate actin, Sec6, the plasma membrane Ca2+ pump, the G protein subunits Gαq and Gβγ, the β1 isoform of phospholipase C, and the ER resident IP3R1 from brain microsomal extracts. Antibodies against the various signaling and Ca2+ transport proteins coimmunoprecipitate Sec8 and the other signaling proteins. Dissociation of actin filaments in the immunoprecipitate had no effect on the interaction between Sec6 and Sec8, but released the actin and dissociated the interaction between the Sec6/8 complex and Ca2+ signaling proteins. Hence, the interaction between the Sec6/8 and Ca2+ signaling complexes is likely mediated by the actin cytoskeleton. The anti-Sec6 and anti-Sec8 antibodies inhibited Ca2+ signaling at a step upstream of Ca2+ release by IP3. Disruption of the actin cytoskeleton with latrunculin B in intact cells resulted in partial translocation of Sec6 and Sec8 from membranes to the cytosol and interfered with propagation of agonist-evoked Ca2+ waves. Our results suggest that the Sec6/8 complex has multiple roles in secretory cells including governing the polarized expression of Ca2+ signaling complexes and regulation of their activity.

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