Role of Membrane-tension Gated Ca Flux in Cell Mechanosensation

He, Lijuan; Tao, Jiaxiang; Si, Fangwei; Wu, Yi; Wu, Tung‐Kung; Prasath, Vishnu; Wirtz, Denis; Sun, Sean X.

doi:10.1101/134395

Cited by 6 publications

(8 citation statements)

References 45 publications

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“…Membrane tension affects cell migration (Gauthier et al, 2011; Houk et al, 2012; Keren et al, 2008; Mueller et al, 2017), vesicle fusion and recycling (Boulant et al, 2011; Gauthier et al, 2011; Maritzen and Haucke, 2017; Masters et al, 2013; Shillcock and Lipowsky, 2005; Shin et al, 2018; Thottacherry et al, 2017; Wen et al, 2016), the cell cycle (Stewart et al, 2011), cell signaling (Basu et al, 2016; Groves and Kuriyan, 2010; Houk et al, 2012; Huse, 2017; Romer et al, 2007), and mechanosensation (He et al, 2018; Phillips et al, 2009; Ranade et al, 2015). However, there has been controversy over the speed and degree to which localized changes in membrane tension propagate in cells (Diz-Muñoz et al, 2013).…”

Section: Introductionmentioning

confidence: 99%

Cell Membranes Resist Flow

Shi

Graber

Baumgart

et al. 2018

Cell

306

292

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SUMMARY The fluid-mosaic model posits a liquid-like plasma membrane, which can flow in response to tension gradients. It is widely assumed that membrane flow transmits local changes in membrane tension across the cell in milliseconds, mediating long-range signaling. Here we show that propagation of membrane tension occurs quickly in cell-attached blebs, but is largely suppressed in intact cells. The failure of tension to propagate in cells is explained by a fluid dynamical model that incorporates the flow resistance from cytoskeleton-bound transmembrane proteins. Perturbations to tension propagate diffusively, with a diffusion coefficient Dσ ~ 0.024 μm2/s in HeLa cells. In primary endothelial cells, local increases in membrane tension lead only to local activation of mechanosensitive ion channels and to local vesicle fusion. Thus membrane tension is not a mediator of long-range intra-cellular signaling, but local variations in tension mediate distinct processes in sub-cellular domains.

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Section: Introductionmentioning

confidence: 99%

Cell Membranes Resist Flow

Shi

Graber

Baumgart

et al. 2018

Cell

306

292

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“…As Rho GTPase activity drives actomyosin-mediated mechanical forces, mechanical forces also in turn modulate Rho GTPase activity via mechanotransduction: for example, mechanical compression of the cell membrane in human mesenchymal cells has been shown to reduce RhoA activity, mediated by mechanosensitive ion channels (14). Katsumi et al (15) show that the stretch of vascular smooth muscle cells inhibited Rac and decreased lamellipodia formation.…”

Section: Introductionmentioning

confidence: 99%

Mechanochemical Coupling and Junctional Forces during Collective Cell Migration

Bui

Conway

Heise

et al. 2019

Biophysical Journal

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Cell migration, a fundamental physiological process in which cells sense and move through their surrounding physical environment, plays a critical role in development and tissue formation, as well as pathological processes, such as cancer metastasis and wound healing. During cell migration, dynamics are governed by the bidirectional interplay between cell-generated mechanical forces and the activity of Rho GTPases, a family of small GTP-binding proteins that regulate actin cytoskeleton assembly and cellular contractility. These interactions are inherently more complex during the collective migration of mechanically coupled cells because of the additional regulation of cell-cell junctional forces. In this study, we adapted a recent minimal modeling framework to simulate the interactions between mechanochemical signaling in individual cells and interactions with cell-cell junctional forces during collective cell migration. We find that migration of individual cells depends on the feedback between mechanical tension and Rho GTPase activity in a biphasic manner. During collective cell migration, waves of Rho GTPase activity mediate mechanical contraction/extension and thus synchronization throughout the tissue. Further, cell-cell junctional forces exhibit distinct spatial patterns during collective cell migration, with larger forces near the leading edge. Larger junctional force magnitudes are associated with faster collective cell migration and larger tissue size. Simulations of heterogeneous tissue migration exhibit a complex dependence on the properties of both leading and trailing cells. Computational predictions demonstrate that collective cell migration depends on both the emergent dynamics and interactions between cellular-level Rho GTPase activity and contractility and multicellular-level junctional forces. the direction of migration (5,6).At the level of an individual cell, although there are many signaling pathways that regulate the dynamics of lamellipodia and filopodia cellular extensions, Rho GTPases are key drivers of this process. Rho GTPases are small GTP-binding proteins that regulate essential cellular processes and functions, including cellular adhesion, shape, and proliferation.

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“…Actin dynamics and cortical contractile stress can also affect cell volume through multiple mechanisms such as vesicle transport and tension-activated channels [39,40]. In this paper we found that the actin cortex, on average, had a small effect on HN31 cell volume.…”

Section: Discussionmentioning

confidence: 64%

Electromechanics and Volume Dynamics in Non-excitable Tissue Cells

Yellin

Sreenivasan³

et al. 2018

Preprint

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Cell volume regulation is fundamentally important in phenomena such as cell growth, proliferation, tissue homeostasis and embryogenesis. How the cell size is set, maintained, and changed over a cell's lifetime is not well understood. In this work we focus on how the volume of non-excitable tissue cells is coupled to the cell membrane electrical potential and the concentration of membrane-permeable ions in the cell environment. Specifically, we demonstrate that a sudden cell depolarization using the whole cell patch clamp results in a 30 percent increase in cell volume, while hyperpolarization results in a slight volume decrease. We find that cell volume can be partially controlled by changing the chloride or the sodium/potassium concentrations in the extracellular environment while maintaining a constant external osmotic pressure. Depletion of external chloride leads to a volume decrease in suspended HN31 cells.Introducing cells to a high potassium solution causes volume increase by up to 50%. Cell volume is also influenced by cortical tension: actin depolymerization leads to cell volume increase. We present an electrophysiology model of water dynamics driven by changes in membrane potential and in the concentration of permeable ions in the cell surrounding. The model quantitatively predicts that the cell volume is determined by the total amount of intracellular ion and protein content.

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Role of Membrane-tension Gated Ca Flux in Cell Mechanosensation

Cited by 6 publications

References 45 publications

Cell Membranes Resist Flow

Cell Membranes Resist Flow

Mechanochemical Coupling and Junctional Forces during Collective Cell Migration

Electromechanics and Volume Dynamics in Non-excitable Tissue Cells

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