Animal Cell Hydraulics http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2736862/

[Lindsay]

Animal Cell Hydraulics By Guillaume T. Charras, Timothy J. Mitchison,
and L. Mahadevan

Water is the dominant ingredient of cells and its dynamics are crucial
to life. We and others have suggested a physical picture of the cell
as a soft, fluid-infiltrated sponge, surrounded by a water-permeable
barrier. To understand water movements in an animal cell, we imposed
an external, inhomogeneous osmotic stress on cultured cancer cells.
This forced water through the membrane on one side, and out on the
other. Inside the cell, it created a gradient in hydration, that we
visualized by tracking cellular responses using natural organelles and
artificially introduced quantum dots. The dynamics of these markers at
short times were the same for normal and metabolically poisoned cells,
indicating that the cellular responses are primarily physical rather
than chemical. Our finding of an internal gradient in hydration is
inconsistent with a continuum model for cytoplasm, but consistent with
the sponge model, and implies that the effective pore size of the
sponge is small enough to retard water flow significantly on time
scales (∼10–100 seconds) relevant to cell physiology. We interpret
these data in terms of a theoretical framework that combines mechanics
and hydraulics in a multiphase poroelastic description of the
cytoplasm and explains the experimentally observed dynamics
quantitatively in terms of a few coarse-grained parameters that are
based on microscopically measurable structural, hydraulic and
mechanical properties. Our fluid-filled sponge model could provide a
unified framework to understand a number of disparate observations in
cell morphology and motility.

[Lindsay]

related: http://www.seas.harvard.edu/softmat/downloads/2008-11.pdf

Two views have dominated recent discussions of the physical basis of
cell shape change during migration and division of animal cells: the
cytoplasm can be modeled as a viscoelastic continuum, and the forces
that change its shape are generated only by actin polymerization and
actomyosin contractility in the cell cortex. Here, we question both
views: we suggest that the cytoplasm is better described as
poroelastic, and that
hydrodynamic forces may be generally important for its shape dynamics.
In the poroelastic view, the cytoplasm consists of a porous, elastic
solid
(cytoskeleton, organelles, ribosomes) penetrated by an interstitial
fluid (cytosol) that moves through the pores in response to pressure
gradients. If
the pore size is small (30–60 nm), as has been observed in some cells,
pressure does not globally equilibrate on time and length scales
relevant to
cell motility. Pressure differences across the plasma membrane drive
blebbing, and potentially other type of protrusive motility. In the
poroelastic
view, these pressures can be higher in one part of a cell than
another, and can thus cause local shape change. Local pressure
transients could
be generated by actomyosin contractility, or by local activation of
osmogenic ion transporters in the plasma membrane. We propose that
local
activation of Na+/H+ antiporters (NHE1) at the front of migrating
cells promotes local swelling there to help drive protrusive motility,
acting in
combination with actin polymerization. Local shrinking at the equator
of dividing cells may similarly help drive invagination during
cytokinesis,
acting in combination with actomyosin contractility. Testing these
hypotheses is not easy, as water is a difficult analyte to track, and
will require a
joint effort of the cytoskeleton and ion physiology communities.