The Arp2/3 complex controls the wave of F-actin on the fused granules and their integration into the APM. (A–D) ARPC2^{fl/fl Mist1-Cre, mT/mG} (A and B left panels, C and D) or Ctrl^{Mist1-Cre, mT/mG} (A and B right panels) were treated with TMX. After 4 wk, salivary glands were exposed, mice were injected with 0.01 mg/kg ISOP and imaged by ISMic (A–C) or processed for indirect immunofluorescence, labeled with Alexa-647 phalloidin, and antibodies were directed against NMIIA and imaged by spinning disk (D). (A) Granules in ARPC2^−/− and ARPC2^+/+ acinar cells (arrows). Bar, 5 µm. (B) ISMic time-lapse of granule integration. Bar, 1 µm. (C) Time course of granule integration was measured in ARPC2^−/− (green solid symbols) and ARPC2^+/+ (green open symbols) cells. Data are averages ± SD. (ARPC2^−/−: N = 44 granules, 18 cells, 4 animals; ARPC2^+/+: N = 61 granules, 24 cells, 5 animals). (D) Phalloidin and NMIIA staining of granules at early and later stages of integration. Bar, 1 µm. (E–G) GFP-LF/mTom (E and F) or WT (G) mice were treated with 200 μm CK666 or DMSO (vehicle) and injected with 0.01 mg/kg ISOP. Salivary glands were either imaged by ISMic (E and F) or processed for indirect immunofluorescence labelled with Alexa-647 phalloidin and antibodies directed against mDia1, Arpc2, or NMIIA, and imaged by spinning disk (G). (E) Time course of granule integration was measured for CK666- (green solid symbols) and vehicle-treated (DMSO, green open symbols) cells. Data are averages ± SD. (CK666: N = 44 granules, 19 cells, 5 animals; DMSO: N = 48 granules, 16 cells, 5 animals). Bar, 1 µm. (H) Model of the effect of Arp2/3 inhibition on granule integration.