To migrate or to degranulate, that is the question
To avoid loss of their munitions before reaching their final destination at inflamed sites, mature MCs need to be regulated to migrate, but not yet degranulate (Figure 3). This is a challenging requirement as some of the MC chemokines induce degranulation of basophils 77and synergize with secretagogues to potentiate MC degranulation78,79. Thus, it was proposed that chemokines may either elicit distinct signals in MCs, as opposed to basophils, or that MC SGs are linked to the cell cytoskeleton differently from the basophil granules 77. Marked differences observed between the actin skeleton in migrating versus secreting MCs support the latter possibility 80. Analysis of actin rearrangements following chemokine stimulation of MCs revealed an accumulation of pericentral actin clusters that prevent cell flattening and converge the SGs in the cell center 80. By contrast, reduction in the actin mesh density characterizes the secretory actin phenotype. Thus, the migratory actin phenotype immobilizes the secretory granules by trapping them in the cell center, whereas the secretory actin phenotype supports mobility and exocytosis. Diaphanous-related formin, mDia1, appears to be key player in these actin rearrangements 80 (Figure 3).