Unknown

Dataset Information

0

Actin-Membrane Release Initiates Cell Protrusions.


ABSTRACT: Despite the well-established role of actin polymerization as a driving mechanism for cell protrusion, upregulated actin polymerization alone does not initiate protrusions. Using a combination of theoretical modeling and quantitative live-cell imaging experiments, we show that local depletion of actin-membrane links is needed for protrusion initiation. Specifically, we show that the actin-membrane linker ezrin is depleted prior to protrusion onset and that perturbation of ezrin's affinity for actin modulates protrusion frequency and efficiency. We also show how actin-membrane release works in concert with actin polymerization, leading to a comprehensive model for actin-driven shape changes. Actin-membrane release plays a similar role in protrusions driven by intracellular pressure. Thus, our findings suggest that protrusion initiation might be governed by a universal regulatory mechanism, whereas the mechanism of force generation determines the shape and expansion properties of the protrusion.

SUBMITTER: Welf ES 

PROVIDER: S-EPMC7908823 | biostudies-literature |

REPOSITORIES: biostudies-literature

Similar Datasets

| S-EPMC8283920 | biostudies-literature
| S-EPMC3631436 | biostudies-literature
| S-EPMC9565809 | biostudies-literature
| S-EPMC4359926 | biostudies-literature
| S-EPMC3543002 | biostudies-literature
| S-EPMC7407079 | biostudies-literature
| S-EPMC10173786 | biostudies-literature
| S-EPMC10330871 | biostudies-literature
| S-EPMC9340795 | biostudies-literature
| S-EPMC4070382 | biostudies-literature