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Effect of Cytoskeleton Elasticity on Amoeboid Swimming.

ABSTRACT: Recently, it has been reported that the cells of the immune system, as well as Dictyostelium amoebae, can swim in a bulk fluid by changing their shape repeatedly. We refer to this motion as amoeboid swimming. Here, we explore how the propulsion and the deformation of the cell emerge as an interplay between the active forces that the cell employs to activate the shape changes and the passive, viscoelastic response of the cell membrane, the cytoskeleton, and the surrounding environment. We introduce a model in which the cell is represented by an elastic capsule enclosing a viscous liquid. The motion of the cell is activated by time-dependent forces distributed along its surface. The model is solved numerically using the boundary integral formulation. The cell can swim in a fluid medium using cyclic deformations or strokes. We measure the swimming velocity of the cell as a function of the force amplitude, the stroke frequency, and the viscoelastic properties of the cell and the medium. We show that an increase in the shear modulus leads both to a regular slowdown of the swimming, which is more pronounced for more deflated swimmers, and to a tendency toward cell buckling. For a given stroke frequency, the swimming velocity shows a quadratic dependence on force amplitude for small forces, as expected, but saturates for large forces. We propose a scaling relationship for the dependence of swimming velocity on the relevant parameters that qualitatively reproduces the numerical results and allows us to define regimes in which the cell motility is dominated by elastic response or by the effective cortex viscosity. This leads to an estimate of the effective cortex viscosity of 103 Pa ? s for which the two effects are comparable, which is close to that provided by several experiments.

SUBMITTER: Ranganathan M

PROVIDER: S-EPMC6170896 | biostudies-literature | 2018 Oct

REPOSITORIES: biostudies-literature

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Effect of Cytoskeleton Elasticity on Amoeboid Swimming.

Ranganathan Madhav M Farutin Alexander A Misbah Chaouqi C

Biophysical journal 20180816 7

Recently, it has been reported that the cells of the immune system, as well as Dictyostelium amoebae, can swim in a bulk fluid by changing their shape repeatedly. We refer to this motion as amoeboid swimming. Here, we explore how the propulsion and the deformation of the cell emerge as an interplay between the active forces that the cell employs to activate the shape changes and the passive, viscoelastic response of the cell membrane, the cytoskeleton, and the surrounding environment. We introdu ...[more]

PMID: 30177444

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Project description:Myelin surrounding central nervous system (CNS) axons breaks down in multiple sclerosis (MS) and following traumatic axonal injury. Myelin-debris so produced is harmful to repair since it impedes remyelination in MS and the regeneration of traumatized axons. These devastating outcomes are largely due to inefficient removal by phagocytosis of myelin-debris by microglia. Therefore, revealing mechanisms that control phagocytosis is vital. We previously showed that in phagocytosis, filopodia and lamellipodia extend/engulf and then retract/internalize myelin-debris. Moreover, cofilin activates phagocytosis by advancing the remodeling of actin filaments (i.e., existing filaments disassemble and new filaments assemble in a new configuration), causing filopodia/lamellipodia to protrude, and furthermore, Galectin-3 (formally named MAC-2) activates phagocytosis by enhancing K-Ras.GTP/PI3K signaling that leads to actin/myosin-based contraction, causing filopodia/lamellipodia to retract. To understand further how Galectin-3 controls phagocytosis we knocked-down (KD) Galectin-3 expression in cultured primary microglia using Galectin-3 small-hairpin RNA (Gal-3-shRNA). KD Galectin-3 protein levels reduced phagocytosis extensively. Further, inhibiting nucleolin (NCL) and nucleophosmin (NPM), which advance K-Ras signaling as does Galectin-3, also reduced phagocytosis. Strikingly and unexpectedly, knocking down Galectin-3 resulted in a dramatic transformation of microglia morphology from "amoeboid-like" to "branched-like," rearrangement of actin filaments and inactivation of cofilin. Thus, Galectin-3 may control microglia morphology and phagocytosis by regulating the activation state of cofilin, which, in turn, affects how actin filaments organize and how stable they are. Furthermore, our current and previous findings together suggest that Galectin-3 activates phagocytosis by targeting the cytoskeleton twice: first, by advancing cofilin activation, causing filopodia/lamellipodia to extend/engulf myelin-debris. Second, by advancing actin/myosin-based contraction through K-Ras.GTP/PI3K signaling, causing filopodia/lamellipodia to retract/internalize myelin-debris.

Dataset Information

Effect of Cytoskeleton Elasticity on Amoeboid Swimming.

Publications

Effect of Cytoskeleton Elasticity on Amoeboid Swimming.

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