Blebs are spherical membrane protrusions often observed during cell migration, cell spreading, cytokinesis, and apoptosis, both in cultured cells and in vivo.
Bleb expansion is thought to be driven by the contractile
actomyosin cortex, which generates hydrostatic pressure in the cytoplasm and can thus drive herniations of the plasma membrane. However, the role of cortical tension in
bleb formation has not been directly tested, and despite the importance of blebbing, little is known about the mechanisms of
bleb growth. In order to explore the link between cortical tension and
bleb expansion, we induced
bleb formation on cells with different tensions.
Blebs were nucleated in a controlled manner by
laser ablation of the cortex, mimicking endogenous
bleb nucleation. Cortical tension was modified by treatments affecting the level of
myosin activity or
proteins regulating actin turnover. We show that there is a critical tension below which
blebs cannot expand. Above this threshold, the maximal size of a
bleb strongly depends on tension, and this dependence can be fitted with a model of the cortex as an active elastic material. Together, our observations and model allow us to relate
bleb shape parameters to the underlying cellular mechanics and provide insights as to how
bleb formation can be biochemically regulated during cell motility.