The application of high and super-resolution microscopy techniques has extended the possibilities of studying actin dynamics in mast cells (MCs). These studies demonstrated the close correlation between actin-driven changes in cell morphology and the functions that MC perform during their life cycle. Dynamic conversions between actin polymerization and depolymerization support MC degranulation and leading to the release of the preformed, secretory granule (SG)-contained, inflammatory mediators. Cell flattening inflicting an actin porous geometry and clearing of cortical actin, characterize the secretory actin phenotype. In contrast, pericentral actin clusters, that entrap the SGs, characterize the migratory actin phenotype, which supports MC migration, but restricts MC degranulation. Multiple actin binding and actin interacting proteins regulate these actin rearrangements, in compliance with the signals elicited by the respective activating receptors. Here, we review recent findings on the interplay between the actin cytoskeleton and MC migration and degranulation.