Current models for protrusive motility in animal cells focus on
cytoskeleton-based mechanisms, where localized protrusion is
driven by local regulation of actin biochemistry1–3. In plants and
fungi, protrusion is driven primarily by hydrostatic pressure4–6.
For hydrostatic pressure to drive localized protrusion in animal
cells7,8, it would have to be locally regulated, but current models
treating cytoplasm as an incompressible viscoelastic continuum9
or viscous liquid10 require that hydrostatic pressure equilibrates
essentially instantaneously over the whole cell. Here, we use cell
blebs as reporters of local pressure in the cytoplasm. When we
locally perfuse blebbing cells with cortex-relaxing drugs to dissipate pressure on one side, blebbing continues on the untreated
side, implying non-equilibration of pressure on scales of approximately 10 mm and 10 s. We can account for localization of pressure
by considering the cytoplasm as a contractile, elastic network
infiltrated by cytosol. Motion of the fluid relative to the network
generates spatially heterogeneous transients in the pressure field,
and can be described in the framework of poroelasticity11,12.