Relation between cell activity and the distribution of cytoplasmic actin and myosin.

Herman, Ira M.; Crisona, Nancy J.; Pollard, T.D.

doi:10.1083/jcb.90.1.84

Cited by 218 publications

(109 citation statements)

References 39 publications

(50 reference statements)

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“…Although stress fibers are most prominent in static cells (11), they are nevertheless capable of undergoing dynamic reorganization in motile cells. The observations made in this study clearly illustrate how the organization of stress fibers can change and thus coordinate with the translocation of the cell.…”

Section: Discussionmentioning

confidence: 99%

Reorganization of actin filament bundles in living fibroblasts.

Wang¹

1984

The Journal of Cell Biology

141

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We investigated how actin bundles assemble, disassemble, and reorganize during cell movement. Living chick embryonic fibroblasts were microinjected with actin molecules that had been fluorescently labeled with tetramethylrhodamine. We found that the fluorescent analogue of actin can be used successfully by both existing and newly formed cellular structures. Using time-lapse photography coupled to image-intensified fluorescence microscopy, we were able to detect various patterns of reorganization in motile cells~ Assembly of stress fibers occurred near both the leading and the trailing ends of the cell. The initial structure appeared as discrete spots that subsequently extended into stress fibers. The extension occurred unidirectionally. The site of initiation near the leading edge remained stationary relative to the substrate during subsequent cell advancement. However, the orientation of the fiber could change according to the direction of cell movement. In addition, existing stress fibers could merge or fragment. The shortening of stress fibers can occur from either end of the fiber. Shortening from the proximal end (centrifugal shortening) was accompanied by a decrease in fluorescence intensity, as if the bundle were disassembling, and usually led to the total disappearance of the bundle. Shortening from the distal end (centripetal shortening), on the other hand, is usually accompanied by an increase in fluorescence intensity at the distal end of the bundle, as if this end had pulled loose from its attachment and retracted toward the center of the cell. Besides stress fibers, arc-like actin bundles have also been detected in spreading cells. These observations can explain how the organization of actin bundles coordinates with cell movement, and how stress fibers reach a highly regular pattern in static cells.Light and electron microscopic studies have clearly demonstrated the presence of actin bundles in nonmuscle cells (2). The most prominent class, stress fibers, contain a number of accessory proteins such as alpha-actinin, tropomyosin, and myosin, arranged in a regular pattern somewhat similar to that in myofibrils (7,14,18). At least one end of the stress fiber is usually attached to the membrane, opposite to the site of adhesion plaque on the external surface (10, 12). Besides stress fibers, actin bundles have also been identified in the "arcs" of spreading cells (9,20) and in microvilli (26).Although these different types of bundles probably represent different structures and probably serve different functions, they share a common characteristic: the ability to reorganize. For example, "arcs" form near the leading edge of the cell, then move toward the nucleus and disappear (9,20). Stress fibers exhibit a drastic reorientation when cells are placed in an electric field (16). Even in relatively static cells, changes in the organization of actin bundles have been detected (29). This is not surprising in view of the highly dynamic nature of the actin filaments, which are capable of polymerization-...

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Section: Discussionmentioning

confidence: 99%

Reorganization of actin filament bundles in living fibroblasts.

Wang¹

1984

The Journal of Cell Biology

141

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“…The process may be regulated by the rates of actin nucleation, elongation, dissociation, and possibly myosin-dependent forces that pull on actin filaments (Medeiros et al, 2006). The dependence of the flux on cell migration and mechanical signals explains why prominent stress fibers are present only in relatively immotile cells (Herman et al, 1981;Tomasek et al, 1982), and in cells on stiff substrates (Pelham and Wang, 1997).…”

Section: Discussionmentioning

confidence: 99%

Retrograde Fluxes of Focal Adhesion Proteins in Response to Cell Migration and Mechanical Signals

Guo

Wang

2007

MBoC

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Recent studies suggest that mechanical signals mediated by the extracellular matrix play an essential role in various physiological and pathological processes; yet, how cells respond to mechanical stimuli remains elusive. Using live cell fluorescence imaging, we found that actin filaments, in association with a number of focal adhesion proteins, including zyxin and vasodilator-stimulated phosphoprotein, undergo retrograde fluxes at focal adhesions in the lamella region. This flux is inversely related to cell migration, such that it is amplified in fibroblasts immobilized on micropatterned islands. In addition, the flux is regulated by mechanical signals, including stretching forces applied to flexible substrates and substrate stiffness. Conditions favoring the flux share the common feature of causing large retrograde displacements of the interior actin cytoskeleton relative to the substrate anchorage site, which may function as a switch translating mechanical input into chemical signals, such as tyrosine phosphorylation. In turn, the stimulation of actin flux at focal adhesions may function as part of a feedback mechanism, regulating structural assembly and force production in relation to cell migration and mechanical load. The retrograde transport of associated focal adhesion proteins may play additional roles in delivering signals from focal adhesions to the interior of the cell. INTRODUCTIONRecent studies suggest that mechanosensing is involved in several physiological processes, including embryogenesis (Newman and Comper, 1990;Beloussov et al., 1994) and wound healing (Hinz et al., 2001;Tomasek et al., 2002), and in pathological processes such as fibrosis and carcinogenesis (Paszek et al., 2005). Adherent cells seem capable of both responding to applied mechanical forces (Tzima et al., 2005) and applying contractile forces to probe mechanical properties of the environment (Discher et al., 2005). The downstream responses include changes in migration (Pelham and Wang, 1997;Sheetz et al., 1998;Lo et al., 2000), cell-cell interactions (Guo et al., 2006), proliferation (Wang et al., 2000Nelson et al., 2005), differentiation (Engler et al., 2004(Engler et al., , 2006, and apoptosis . For cultured adherent cells, focal adhesions are thought to mediate mechanosensing through integrin-mediated anchorage to the extracellular matrix (Larsen et al., 2006). The molecular repertoire of focal adhesions includes Ͼ100 adaptor and signaling proteins (Bershadsky et al., 2006), in addition to associated actomyosin bundles that provide mechanical forces for probing the environment (Choquet et al., 1997), inside-out signaling (Chrzanowska-Wodnicka and Burridge, 1996;Schwartz and Ginsberg, 2002), and cell migration (Ridley et al., 2003). However, few details are available concerning how these components work in concert to generate the responses to mechanical signals.Several aspects have emerged recently as the key features of integrin-mediated mechanosensing. First is the increase in cortical organization and contractility in resp...

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“…1D) and, thus, are missing from the cell cortex and endoplasm. It is important not to define the mesenchymal cell on the basis of the presence of stress fibers, because these are abnormal cells that do not actively migrate (Herman et al, 1981;Tomasek et al, 1982). Moreover, the Rho A and MEK pathways (Bhowmick et al, 2001;Roberts, 2002) that produce stress fibers do not produce true EMT in vivo (Nawshad and Hay, 2003).…”

Section: Embryonic Emt Produces Migrating Cells Not Stress Fibersmentioning

confidence: 99%

The mesenchymal cell, its role in the embryo, and the remarkable signaling mechanisms that create it

Hay

2005

Developmental Dynamics

565

478

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This review centers on the role of the mesenchymal cell in development. The creation of this cell is a remarkable process, one where a tightly knit, impervious epithelium suddenly extends filopodia from its basal surface and gives rise to migrating cells. The ensuing process of epithelial-mesenchymal transformation (EMT) creates the mechanism that makes it possible for the mesenchymal cell to become mobile, so as to leave the epithelium and move through the extracellular matrix. EMT is now recognized as a very important mechanism for the remodeling of embryonic tissues, with the power to turn an epithelial somite into sclerotome mesenchyme, and the neural crest into mesenchyme that migrates to many targets. Thus, the time has come for serious study of the underlying mechanisms and the signaling pathways that are used to form the mesenchymal cell in the embryo. In this review, I discuss EMT centers in the embryo that are ready for such serious study and review our current understanding of the mechanisms used for EMT in vitro, as well as those that have been implicated in EMT in vivo. The purpose of this review is not to describe every study published in this rapidly expanding field but rather to stimulate the interest of the reader in the study of the role of the mesenchymal cell in the embryo, where it plays profound roles in development. In the adult, mesenchymal cells may give rise to metastatic tumor cells and other pathological conditions that we will touch on at the end of the review. Developmental Dynamics 233:706 -720, 2005.

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Relation between cell activity and the distribution of cytoplasmic actin and myosin.

Cited by 218 publications

References 39 publications

Reorganization of actin filament bundles in living fibroblasts.

Reorganization of actin filament bundles in living fibroblasts.

Retrograde Fluxes of Focal Adhesion Proteins in Response to Cell Migration and Mechanical Signals

The mesenchymal cell, its role in the embryo, and the remarkable signaling mechanisms that create it

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