10 research outputs found
Maximal fluctuations of confined actomyosin gels: dynamics of the cell nucleus
We investigate the effect of stress fluctuations on the stochastic dynamics
of an inclusion embedded in a viscous gel. We show that, in non-equilibrium
systems, stress fluctuations give rise to an effective attraction towards the
boundaries of the confining domain, which is reminiscent of an active Casimir
effect. We apply this generic result to the dynamics of deformations of the
cell nucleus and we demonstrate the appearance of a fluctuation maximum at a
critical level of activity, in agreement with recent experiments [E. Makhija,
D. S. Jokhun, and G. V. Shivashankar, Proc. Natl. Acad. Sci. U.S.A. 113, E32
(2016)].Comment: 12 pages, 5 figure
Soft inclusion in a confined fluctuating active gel
We study stochastic dynamics of a point and extended inclusion within a one
dimensional confined active viscoelastic gel. We show that the dynamics of a
point inclusion can be described by a Langevin equation with a confining
potential and multiplicative noise. Using a systematic adiabatic elimination
over the fast variables, we arrive at an overdamped equation with a proper
definition of the multiplicative noise. To highlight various features and to
appeal to different biological contexts, we treat the inclusion in turn as a
rigid extended element, an elastic element and a viscoelastic (Kelvin-Voigt)
element. The dynamics for the shape and position of the extended inclusion can
be described by coupled Langevin equations. Deriving exact expressions for the
corresponding steady state probability distributions, we find that the active
noise induces an attraction to the edges of the confining domain. In the
presence of a competing centering force, we find that the shape of the
probability distribution exhibits a sharp transition upon varying the amplitude
of the active noise. Our results could help understanding the positioning and
deformability of biological inclusions, eg. organelles in cells, or nucleus and
cells within tissues.Comment: 16 pages, 9 figure
Mechanochemical feedback control of dynamin independent endocytosis modulates membrane tension in adherent cells.
Plasma membrane tension regulates many key cellular processes. It is modulated by, and can modulate, membrane trafficking. However, the cellular pathway(s) involved in this interplay is poorly understood. Here we find that, among a number of endocytic processes operating simultaneously at the cell surface, a dynamin independent pathway, the CLIC/GEEC (CG) pathway, is rapidly and specifically upregulated upon a sudden reduction of tension. Moreover, inhibition (activation) of the CG pathway results in lower (higher) membrane tension. However, alteration in membrane tension does not directly modulate CG endocytosis. This requires vinculin, a mechano-transducer recruited to focal adhesion in adherent cells. Vinculin acts by controlling the levels of a key regulator of the CG pathway, GBF1, at the plasma membrane. Thus, the CG pathway directly regulates membrane tension and is in turn controlled via a mechano-chemical feedback inhibition, potentially leading to homeostatic regulation of membrane tension in adherent cells
Breakdown of effective temperature, power law interactions, and self-propulsion in a momentum-conserving active fluid
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Mechanochemical feedback control of dynamin independent endocytosis modulates membrane tension in adherent cells.
A mechano-osmotic feedback couples cell volume to the rate of cell deformation
Mechanics has been a central focus of physical biology in the past decade. In comparison, the osmotic and electric properties of cells are less understood. Here we show that a parameter central to both the physics and the physiology of the cell, its volume, depends on a mechano-osmotic coupling. We found that cells change their volume depending on the rate at which they change shape, when they spread, migrate or are externally deformed. Cells undergo slow deformation at constant volume, while fast deformation leads to volume loss. We propose a mechano-sensitive pump and leak model to explain this phenomenon. Our model and experiments suggest that volume modulation depends on the state of the actin cortex and the coupling of ion fluxes to membrane tension. This mechano-osmotic coupling defines a membrane tension homeostasis module constantly at work in cells, causing volume fluctuations associated with fast cell shape changes, with potential consequences on cellular physiology
A mechano-osmotic feedback couples cell volume to the rate of cell deformation
International audienceMechanics has been a central focus of physical biology in the past decade. In comparison, how cells manage their size is less understood. Here, we show that a parameter central to both the physics and the physiology of the cell, its volume, depends on a mechano-osmotic coupling. We found that cells change their volume depending on the rate at which they change shape, when they spontaneously spread or when they are externally deformed. Cells undergo slow deformation at constant volume, while fast deformation leads to volume loss. We propose a mechanosensitive pump and leak model to explain this phenomenon. Our model and experiments suggest that volume modulation depends on the state of the actin cortex and the coupling of ion fluxes to membrane tension. This mechano-osmotic coupling defines a membrane tension homeostasis module constantly at work in cells, causing volume fluctuations associated with fast cell shape changes, with potential consequences on cellular physiology
A mechano-osmotic feedback couples cell volume to the rate of cell deformation
Abstract Mechanics has been a central focus of physical biology in the past decade. In comparison, the osmotic and electric properties of cells are less understood. Here we show that a parameter central to both the physics and the physiology of the cell, its volume, depends on a mechano-osmotic coupling. We found that cells change their volume depending on the rate at which they change shape, when they spread, migrate or are externally deformed. Cells undergo slow deformation at constant volume, while fast deformation leads to volume loss. We propose a mechano-sensitive pump and leak model to explain this phenomenon. Our model and experiments suggest that volume modulation depends on the state of the actin cortex and the coupling of ion fluxes to membrane tension. This mechano-osmotic coupling defines a membrane tension homeostasis module constantly at work in cells, causing volume fluctuations associated with fast cell shape changes, with potential consequences on cellular physiology
Mechanochemical feedback control of dynamin independent endocytosis modulates membrane tension in adherent cells
Plasma membrane tension regulates many key cellular processes. It is modulated by, and can modulate, membrane trafficking. However, the cellular pathway(s) involved in this interplay is poorly understood. Here we find that, among a number of endocytic processes operating simultaneously at the cell surface, a dynamin independent pathway, the CLIC/GEEC (CG) pathway, is rapidly and specifically upregulated upon a sudden reduction of tension. Moreover, inhibition (activation) of the CG pathway results in lower (higher) membrane tension. However, alteration in membrane tension does not directly modulate CG endocytosis. This requires vinculin, a mechano-transducer recruited to focal adhesion in adherent cells. Vinculin acts by controlling the levels of a key regulator of the CG pathway, GBF1, at the plasma membrane. Thus, the CG pathway directly regulates membrane tension and is in turn controlled via a mechano-chemical feedback inhibition, potentially leading to homeostatic regulation of membrane tension in adherent cells