Cell motility driven by actin polymerization

Mogilner, Alex; Oster, George

doi:10.1016/s0006-3495(96)79496-1

Cited by 855 publications

(898 citation statements)

References 61 publications

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“…However, because we discretized angles into six possible orientations, our resolution limits our ability to study the precise details of the preferred orientation. (For example, we cannot explain the dominant angular preference around ±30 • ; but see Mogilner and Oster (1996a); Maly and Borisy (2001). )…”

Section: Internal Architecture Of the Cellmentioning

confidence: 85%

Polarization and Movement of Keratocytes: A Multiscale Modelling Approach

et al. 2006

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Section: Internal Architecture Of the Cellmentioning

confidence: 85%

Polarization and Movement of Keratocytes: A Multiscale Modelling Approach

et al. 2006

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“…However, cell body translocation was only partially inhibited by blebbistatin, suggesting that either myosin II activity was not completely blocked by this drug or that there are other redundant mechanisms contributing to the cell body translocation. One of the possibilities is that in the absence of myosin activity the force could be produced by the depolymerization-driven entropic network contraction (Mogilner and Oster, 1996). Regardless, fragmentation of the cell suggested that when myosin activity was attenuated, cell body could not follow front protrusion in a robust and effective way.…”

Section: Molecular Biology Of the Cell 3728mentioning

confidence: 99%

Comparative Maps of Motion and Assembly of Filamentous Actin and Myosin II in Migrating Cells

Schaub

Bohnet

Laurent

et al. 2007

MBoC

120

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To understand the mechanism of cell migration, one needs to know how the parts of the motile machinery of the cell are assembled and how they move with respect to each other. Actin and myosin II are thought to be the major structural and force-generating components of this machinery (Mitchison and Cramer, 1996; Parent, 2004). The movement of myosin II along actin filaments is thought to generate contractile force contributing to cell translocation, but the relative motion of the two proteins has not been investigated. We use fluorescence speckle and conventional fluorescence microscopy, image analysis, and computer tracking techniques to generate comparative velocity and assembly maps of actin and myosin II over the entire cell in a simple model system of persistently migrating fish epidermal keratocytes. The results demonstrate contrasting polarized assembly patterns of the two components, indicate force generation at the lamellipodium-cell body transition zone, and suggest a mechanism of anisotropic network contraction via sliding of myosin II assemblies along divergent actin filaments. INTRODUCTIONCrawling cell motion involves a cycle of several distinct processes: protrusion at the front of the cell, attachment to the substratum, and forward translocation of the cell body followed or accompanied by detachment and withdrawal of the rear of the cell. Crawling motion is thought to be dependent on the actin-myosin II cytoskeletal system (Mitchison and Cramer, 1996): protrusion is thought to be driven by the assembly of actin network, which is anchored to the substratum through integrin-containing adhesions; forward translocation of the cell body and contraction of the rear are thought to depend on the interaction of the actin network with the motor protein myosin II. Actin assembly during the protrusion at the leading edge of motile cells has recently received the most attention both in experimental (Pantaloni et al., 2001;Pollard and Borisy, 2003;Ridley et al., 2003) and theoretical studies (for review, see Mogilner, 2006). In contrast, the mechanisms involved in the forward translocation of the cell body remain largely unclear: the exact layout and the mode of action of the contractile actin-myosin II machinery are controversial. Qualitative models proposed in the literature include shortening of small contractile units similar to muscle sarcomeres, myosin II-dependent transport along uniformly polarized actin arrays, and a dynamic network contraction mechanism where contraction results from alignment of actin filaments by myosin II assemblies (Cramer, 1999;Verkhovsky et al., 1999a). More sophisticated biophysical models aim to understand the contractile cytoskeletal machinery in quantitative physical terms. In the past, considering the cytoskeleton as a gel made of cross-linked semiflexible polymers has helped understanding its passive visco-elastic properties. More recently, attempts were made to develop biophysical models taking into account intrinsic activity of the cytoskeleton: polarized assembly of acti...

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“…In such a 'treadmill' the force of actin polymerization at the front is coupled to the disassembly of the actin network at the rear of the lamellipodia, propelling the leading edge forward along the substrate (Machacek and Danuser, 2006;Pollard and Borisy, 2003;Ponti et al, 2004;Watanabe and Mitchison, 2002). Based on actin filament stiffness, it has been calculated that the 'free' length of the actin filaments pushing the leading edge has to be quite short (less than 150 nm) in order to create sufficient force for membrane protrusion (Mogilner and Oster, 1996), suggesting that the filament length in the treadmill must be very tightly regulated to achieve the most efficient forward movement.…”

Section: Basic Principles Of Cell Migration Overall Structure Of the mentioning

confidence: 99%

Cell biology of embryonic migration

Kurosaka¹,

Kashina²

2008

Birth Defects Research Pt C

113

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Cell migration is an evolutionarily conserved mechanism that underlies the development and functioning of uni-and multicellular organisms and takes place in normal and pathogenic processes, including various events of embryogenesis, wound healing, immune response, cancer metastases, and angiogenesis. Despite the differences in the cell types that take part in different migratory events, it is believed that all of these migrations occur by similar molecular mechanisms, whose major components have been functionally conserved in evolution and whose perturbation leads to severe developmental defects. These mechanisms involve intricate cytoskeleton-based molecular machines that can sense the environment, respond to signals, and modulate the entire cell behavior. A big question that has concerned the researchers for decades relates to the coordination of cell migration in situ and its relation to the intracellular aspects of the cell migratory mechanisms. Traditionally, this question has been addressed by researchers that considered the intra-and extracellular mechanisms driving migration in separate sets of studies. As more data accumulate researchers are now able to integrate all of the available information and consider the intracellular mechanisms of cell migration in the context of the developing organisms that contain additional levels of complexity provided by extracellular regulation. This review provides a broad summary of the existing and emerging data in the cell and developmental biology fields regarding cell migration during development.

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Cell motility driven by actin polymerization

Cited by 855 publications

References 61 publications

Polarization and Movement of Keratocytes: A Multiscale Modelling Approach

Polarization and Movement of Keratocytes: A Multiscale Modelling Approach

Comparative Maps of Motion and Assembly of Filamentous Actin and Myosin II in Migrating Cells

Cell biology of embryonic migration

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