LAMELLIPODIAL AND AMOEBOID CELL LOCOMOTION: THE ROLE OF ACTIN-CYCLING AND BLEB FORMATION

2007 ◽  
Vol 02 (01) ◽  
pp. 5-22 ◽  
Author(s):  
HANS GEORG MANNHERZ ◽  
MONIKA MACH ◽  
DOROTA NOWAK ◽  
MARIA MALICKA-BLASZKIEWICZ ◽  
ANTONINA MAZUR

Cell migration depends on the rapid changes of the organization of actin filaments and generation of force by motor proteins. Vertebrate cells use two different mechanisms: mesenchymal or amoeboid migration. Cells migrating in mesenchymal mode are elongated and move over a two-dimensional substratum. They extend thin veil-like extensions at their leading face — lamellipodia, whose protrusion depend on polymerization and depolymerization processes of actin. During mesenchymal migration actin filaments are firmly connected by integrins to the extracellular matrix (ECM) at focal contacts, which serve as points of fixation for subsequent cell body traction by force producing actomyosin interactions. Cells migrating in amoeboid fashion are rounded and move through a three-dimensional ECM-network undergoing considerable shape changes and generating vesicle-like surface extensions — so-called blebs. These blebs and the migrating cells exhibit no or strongly reduced affinity to the ECM. Bleb formation depends on a transient decrease of plasma membrane stiffness and locally increased hydrostatic pressure, which is generated by actin-myosin interactions. Formation of numerous surface blebs is also typical of cells that undergo apoptotic cell death. Since these share a number of properties to blebs of amoeboid cells, an analysis is given of the distribution of some cytoskeletal components in apoptotic blebs.

2021 ◽  
Vol 41 (01) ◽  
pp. 014-021
Author(s):  
Markus Bender ◽  
Raghavendra Palankar

AbstractPlatelet activation and aggregation are essential to limit blood loss at sites of vascular injury but may also lead to occlusion of diseased vessels. The platelet cytoskeleton is a critical component for proper hemostatic function. Platelets change their shape after activation and their contractile machinery mediates thrombus stabilization and clot retraction. In vitro studies have shown that platelets, which come into contact with proteins such as fibrinogen, spread and first form filopodia and then lamellipodia, the latter being plate-like protrusions with branched actin filaments. However, the role of platelet lamellipodia in hemostasis and thrombus formation has been unclear until recently. This short review will briefly summarize the recent findings on the contribution of the actin cytoskeleton and lamellipodial structures to platelet function.


2021 ◽  
Vol 17 (12) ◽  
Author(s):  
Kara L. Feilich ◽  
J. D. Laurence-Chasen ◽  
Courtney Orsbon ◽  
Nicholas J. Gidmark ◽  
Callum F. Ross

Three-dimensional (3D) tongue movements are central to performance of feeding functions by mammals and other tetrapods, but 3D tongue kinematics during feeding are poorly understood. Tongue kinematics were recorded during grape chewing by macaque primates using biplanar videoradiography. Complex shape changes in the tongue during chewing are dominated by a combination of flexion in the tongue's sagittal planes and roll about its long axis. As hypothesized for humans, in macaques during tongue retraction, the middle (molar region) of the tongue rolls to the chewing (working) side simultaneous with sagittal flexion, while the tongue tip flexes to the other (balancing) side. Twisting and flexion reach their maxima early in the fast close phase of chewing cycles, positioning the food bolus between the approaching teeth prior to the power stroke. Although 3D tongue kinematics undoubtedly vary with food type, the mechanical role of this movement—placing the food bolus on the post-canine teeth for breakdown—is likely to be a powerful constraint on tongue kinematics during this phase of the chewing cycle. The muscular drivers of these movements are likely to include a combination of intrinsic and extrinsic tongue muscles.


1995 ◽  
Vol 128 (5) ◽  
pp. 819-835 ◽  
Author(s):  
D Cox ◽  
J A Ridsdale ◽  
J Condeelis ◽  
J Hartwig

This study extends the observations on the defects in pseudopod formation of ABP-120+ and ABP-120- cells by a detailed morphological and biochemical analysis of the actin based cytoskeleton. Both ABP-120+ and ABP-120- cells polymerize the same amount of F-actin in response to stimulation with cAMP. However, unlike ABP-120+ cells, ABP-120- cells do not incorporate actin into the Triton X-100-insoluble cytoskeleton at 30-50 s, the time when ABP-120 is incorporated into the cytoskeleton and when pseudopods are extended after cAMP stimulation in wild-type cells. By confocal and electron microscopy, pseudopods extended by ABP-120- cells are not as large or thick as those produced by ABP-120+ cells and in the electron microscope, an altered filament network is found in pseudopods of ABP-120- cells when compared to pseudopods of ABP-120+ cells. The actin filaments found in areas of pseudopods in ABP-120+ cells either before or after stimulation were long, straight, and arranged into space filling orthogonal networks. Protrusions of ABP-120- cells are less three-dimensional, denser, and filled with multiple foci of aggregated filaments consistent with collapse of the filament network due to the absence of ABP-120-mediated cross-linking activity. The different organization of actin filaments may account for the diminished size of protrusions observed in living and fixed ABP-120- cells compared to ABP-120+ cells and is consistent with the role of ABP-120 in regulating pseudopod extension through its cross-linking of actin filaments.


Cancers ◽  
2020 ◽  
Vol 12 (5) ◽  
pp. 1136 ◽  
Author(s):  
Ladislav Merta ◽  
Aneta Gandalovičová ◽  
Vladimír Čermák ◽  
Michal Dibus ◽  
Tony Gutschner ◽  
...  

The ability of cancer cells to adopt various migration modes (the plasticity of cancer cell invasiveness) is a substantive obstacle in the treatment of metastasis, yet still an incompletely understood process. We performed a comparison of publicly available transcriptomic datasets from various cell types undergoing a switch between the mesenchymal and amoeboid migration modes. Strikingly, lncRNA MALAT1 (metastasis-associated lung adenocarcinoma transcript 1) was one of three genes that were found upregulated in all amoeboid cells analyzed. Accordingly, downregulation of MALAT1 in predominantly amoeboid cell lines A375m2 and A2058 resulted in decrease of active RhoA (Ras homolog family member A) and was accompanied by the amoeboid-mesenchymal transition in A375m2 cells. Moreover, MALAT1 downregulation in amoeboid cells led to increased cell proliferation. Our work is the first to address the role of MALAT1 in MAT/AMT (mesenchymal to amoeboid transition/amoeboid to mesenchymal transition) and suggests that increased MALAT1 expression is a common feature of amoeboid cells.


eLife ◽  
2021 ◽  
Vol 10 ◽  
Author(s):  
Thibaut Brunet ◽  
Marvin Albert ◽  
William Roman ◽  
Maxwell C Coyle ◽  
Danielle C Spitzer ◽  
...  

Amoeboid cell types are fundamental to animal biology and broadly distributed across animal diversity, but their evolutionary origin is unclear. The closest living relatives of animals, the choanoflagellates, display a polarized cell architecture (with an apical flagellum encircled by microvilli) that resembles that of epithelial cells and suggests homology, but this architecture differs strikingly from the deformable phenotype of animal amoeboid cells, which instead evoke more distantly related eukaryotes, such as diverse amoebae. Here, we show that choanoflagellates subjected to confinement become amoeboid by retracting their flagella and activating myosin-based motility. This switch allows escape from confinement and is conserved across choanoflagellate diversity. The conservation of the amoeboid cell phenotype across animals and choanoflagellates, together with the conserved role of myosin, is consistent with homology of amoeboid motility in both lineages. We hypothesize that the differentiation between animal epithelial and crawling cells might have evolved from a stress-induced switch between flagellate and amoeboid forms in their single-celled ancestors.


Author(s):  
T.D. Pollard ◽  
P. Maupin

In this paper we review some of the contributions that electron microscopy has made to the analysis of actin and myosin from nonmuscle cells. We place particular emphasis upon the limitations of the ultrastructural techniques used to study these cytoplasmic contractile proteins, because it is not widely recognized how difficult it is to preserve these elements of the cytoplasmic matrix for electron microscopy. The structure of actin filaments is well preserved for electron microscope observation by negative staining with uranyl acetate (Figure 1). In fact, to a resolution of about 3nm the three-dimensional structure of actin filaments determined by computer image processing of electron micrographs of negatively stained specimens (Moore et al., 1970) is indistinguishable from the structure revealed by X-ray diffraction of living muscle.


1996 ◽  
Vol 34 (1) ◽  
pp. 27
Author(s):  
Sue Yon Shim ◽  
Ki Joon Sung ◽  
Young Ju Kim ◽  
In Soo Hong ◽  
Myung Soon Kim ◽  
...  

2016 ◽  
Vol 2 (2) ◽  
pp. 40
Author(s):  
Miriam Aparicio

This study tests some hypotheses included in the psycho-social-communicational paradigm, which emphasizes the cognitive effects of the media and the role of the psychosocial subject as the recipient


2020 ◽  
Vol 27 ◽  
Author(s):  
Ji-Yeon Lee ◽  
Myoung Hee Kim

: HOX genes belong to the highly conserved homeobox superfamily, responsible for the regulation of various cellular processes that control cell homeostasis, from embryogenesis to carcinogenesis. The abnormal expression of HOX genes is observed in various cancers, including breast cancer; they act as oncogenes or as suppressors of cancer, according to context. In this review, we analyze HOX gene expression patterns in breast cancer and examine their relationship, based on the three-dimensional genome structure of the HOX locus. The presence of non-coding RNAs, embedded within the HOX cluster, and the role of these molecules in breast cancer have been reviewed. We further evaluate the characteristic activity of HOX protein in breast cancer and its therapeutic potential.


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