Figure 1.

Role of the actin cytoskeleton in coordination of BCR signaling and antigen processing functions. BCR signaling triggers actin reorganization as a series of sequential events. An initial transient detachment and disassembly of the cortical actin network is induced by dephosphorylation ezrin and cofilin (A), and a subsequent polarized actin reassembly is mediated in part by Btk-activated WASP (B). The actin remodeling facilitates BCR self-clustering and signaling induction in BCR microclusters. Actin-driven B cell spreading enhances BCR microclustering and signaling (A-B). The transition of actin-mediated cell spreading to contraction promotes the coalescence of BCR microclusters and the formation of the central cluster, which leads to signaling attenuation (C). B cell contraction also likely helps to gather BCR-antigen complexes into endocytosing vesicles. The continuous actin remodeling, the actin adaptor protein Apb1 that couples F-actin with dynamin, and the actin motor non-muscle myosin II (MyoII) are required for the formation and fission of BCR containing budding vesicles from the plasma membrane (D).