Simulating Dictyostelium cell deformation in amoeboid movement

2014 ◽  
Vol 1 ◽  
pp. 25-28
Author(s):  
Shuji Ishihara ◽  
Daisuke Taniguchi ◽  
Satoshi Sawai
Author(s):  
P.L. Moore

Previous freeze fracture results on the intact giant, amoeba Chaos carolinensis indicated the presence of a fibrillar arrangement of filaments within the cytoplasm. A complete interpretation of the three dimensional ultrastructure of these structures, and their possible role in amoeboid movement was not possible, since comparable results could not be obtained with conventional fixation of intact amoebae. Progress in interpreting the freeze fracture images of amoebae required a more thorough understanding of the different types of filaments present in amoebae, and of the ways in which they could be organized while remaining functional.The recent development of a calcium sensitive, demembranated, amoeboid model of Chaos carolinensis has made it possible to achieve a better understanding of such functional arrangements of amoeboid filaments. In these models the motility of demembranated cytoplasm can be controlled in vitro, and the chemical conditions necessary for contractility, and cytoplasmic streaming can be investigated. It is clear from these studies that “fibrils” exist in amoeboid models, and that they are capable of contracting along their length under conditions similar to those which cause contraction in vertebrate muscles.


1965 ◽  
Vol 13 (01) ◽  
pp. 035-046 ◽  
Author(s):  
R. L Henry

SummaryWhite blood cells can no longer be considered simple trapped inclusions within thrombi. Their numbers in thrombi relative to blood counts increase with time. They appear to come from the blood flowing past the thrombus. They appear to migrate by amoeboid movement into the thrombic mass. Polymorphonuclear neutrophils have been shown to be lytic to fibrin and other proteins and thus can contribute to thrombus dissolution. There is increasing evidence that neutrophils may impart important cytotrophic function to proliferating cells during thrombus organization. Eosinophils are known to carr profibrinolysin and will release this precursor at sites of fibrin deposition. Mononuclear leukocytes can transform into fibroblasts in tissue culture and I consider a thrombus an ideal tissue culture medium. All of these cells can contribute to thrombus dissolution simply by mechanical weakening of the mass by migration into it, releasing enzymes, and allowing blood flow to carry away pieces of the thrombus as emboli. I extend my perspective on thrombosis by considering these intravascular solids as cell tissue cultures rather than simple blood clots or platelet aggregates.


2006 ◽  
Vol 128 (6) ◽  
pp. 830-836 ◽  
Author(s):  
Yong-Ping Liu ◽  
Chuan Li ◽  
Kuo-Kang Liu ◽  
Alvin C. K. Lai

In this paper, the mechanical properties of erythrocytes were studied numerically based upon the mechanical model originally developed by Pamplona and Calladine (ASME J. Biomech. Eng., 115, p. 149, 1993) for liposomes. The case under study is the erythrocyte stretched by a pair of laser beams in opposite directions within buffer solutions. The study aims to elucidate the effect of radiation pressure from the optical laser because up to now little is known about its influence on the cell deformation. Following an earlier study by Guck et al. (Phys. Rev. Lett., 84, p. 5451, 2000; Biophys. J., 81, p. 767, 2001), the empirical results of the radiation pressure were introduced and imposed on the cell surface to simulate the real experimental situation. In addition, an algorithm is specially designed to implement the simulation. For better understanding of the radiation pressure on the cell deformation, a large number of simulations were conducted for different properties of cell membrane. Results are first discussed parametrically and then evaluated by comparing with the experimental data reported by Guck et al. An optimization approach through minimizing the errors between experimental and numerical data is used to determine the optimal values of membrane properties. The results showed that an average shear stiffness around 4.611×10-6Nm−1, when the nondimensional ratio of shear modulus to bending modulus ranges from 10 to 300. These values are in a good agreement with those reported in literature.


2020 ◽  
pp. 2002489
Author(s):  
Xinyi Guo ◽  
Mengjie Sun ◽  
Yang Yang ◽  
Huihui Xu ◽  
Ji Liu ◽  
...  

2003 ◽  
Vol 160 (2) ◽  
pp. 267-277 ◽  
Author(s):  
Katarina Wolf ◽  
Irina Mazo ◽  
Harry Leung ◽  
Katharina Engelke ◽  
Ulrich H. von Andrian ◽  
...  

Invasive tumor dissemination in vitro and in vivo involves the proteolytic degradation of ECM barriers. This process, however, is only incompletely attenuated by protease inhibitor–based treatment, suggesting the existence of migratory compensation strategies. In three-dimensional collagen matrices, spindle-shaped proteolytically potent HT-1080 fibrosarcoma and MDA-MB-231 carcinoma cells exhibited a constitutive mesenchymal-type movement including the coclustering of β1 integrins and MT1–matrix metalloproteinase (MMP) at fiber bindings sites and the generation of tube-like proteolytic degradation tracks. Near-total inhibition of MMPs, serine proteases, cathepsins, and other proteases, however, induced a conversion toward spherical morphology at near undiminished migration rates. Sustained protease-independent migration resulted from a flexible amoeba-like shape change, i.e., propulsive squeezing through preexisting matrix gaps and formation of constriction rings in the absence of matrix degradation, concomitant loss of clustered β1 integrins and MT1-MMP from fiber binding sites, and a diffuse cortical distribution of the actin cytoskeleton. Acquisition of protease-independent amoeboid dissemination was confirmed for HT-1080 cells injected into the mouse dermis monitored by intravital multiphoton microscopy. In conclusion, the transition from proteolytic mesenchymal toward nonproteolytic amoeboid movement highlights a supramolecular plasticity mechanism in cell migration and further represents a putative escape mechanism in tumor cell dissemination after abrogation of pericellular proteolysis.


1994 ◽  
Vol 124 (2) ◽  
pp. 123-130 ◽  
Author(s):  
Gerald Weeks ◽  
Cornelis J. Weijer

1999 ◽  
Vol 146 (5) ◽  
pp. 1087-1096 ◽  
Author(s):  
Joseph E. Italiano ◽  
Murray Stewart ◽  
Thomas M. Roberts

The major sperm protein (MSP)-based amoeboid motility of Ascaris suum sperm requires coordinated lamellipodial protrusion and cell body retraction. In these cells, protrusion and retraction are tightly coupled to the assembly and disassembly of the cytoskeleton at opposite ends of the lamellipodium. Although polymerization along the leading edge appears to drive protrusion, the behavior of sperm tethered to the substrate showed that an additional force is required to pull the cell body forward. To examine the mechanism of cell body movement, we used pH to uncouple cytoskeletal polymerization and depolymerization. In sperm treated with pH 6.75 buffer, protrusion of the leading edge slowed dramatically while both cytoskeletal disassembly at the base of the lamellipodium and cell body retraction continued. At pH 6.35, the cytoskeleton pulled away from the leading edge and receded through the lamellipodium as its disassembly at the cell body continued. The cytoskeleton disassembled rapidly and completely in cells treated at pH 5.5, but reformed when the cells were washed with physiological buffer. Cytoskeletal reassembly occurred at the lamellipodial margin and caused membrane protrusion, but the cell body did not move until the cytoskeleton was rebuilt and depolymerization resumed. These results indicate that cell body retraction is mediated by tension in the cytoskeleton, correlated with MSP depolymerization at the base of the lamellipodium.


2009 ◽  
Vol 185 (1) ◽  
pp. 11-19 ◽  
Author(s):  
Farideh Sabeh ◽  
Ryoko Shimizu-Hirota ◽  
Stephen J. Weiss

Tissue invasion during metastasis requires cancer cells to negotiate a stromal environment dominated by cross-linked networks of type I collagen. Although cancer cells are known to use proteinases to sever collagen networks and thus ease their passage through these barriers, migration across extracellular matrices has also been reported to occur by protease-independent mechanisms, whereby cells squeeze through collagen-lined pores by adopting an ameboid phenotype. We investigate these alternate models of motility here and demonstrate that cancer cells have an absolute requirement for the membrane-anchored metalloproteinase MT1-MMP for invasion, and that protease-independent mechanisms of cell migration are only plausible when the collagen network is devoid of the covalent cross-links that characterize normal tissues.


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