fig7
Figure 7. F-actin network controls DCV tethering, transport and secretion at the plasma membrane. (A) F-actins block the access of DCVs to the PM; (B) Actin-severing proteins such as scinderin and gelsolin cut F actins into small filaments, thus facilitating the release of DCV. PI3K causes the depolymerization of F-actins to facilitate the docking of DCVs to the PM; (C) Myosin Va is activated by increased Ca2+ levels during stimulated secretion and interacts with Rab27a and MyRIP on DCVs to facilitate the mobilization of DCVs to the PM. PM: plasma membrane; PI3K: phosphatidylinositol 3 kinase; DCV: dense core vesicles.
