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.