(A) Schematic representation of the contribution of FRM2 in apicoplast inheritance and FRM3 in synchronous division and rosette formation. (B) During invasion, a ring of F-actin translocates with the MJ to the rear of the parasite. Small filaments are likely present within the pellicle and translocated by the actomyosin system to the basal pole, contributing to the F-actin accumulation. (C) Schematic summary of the distribution of F-actin produced at the apical end by FRM1 under the different conditions tested in this study. F-actin either accumulated at the basal end (left), did not show any accumulation (middle), accumulated at the junction between MyoH and MyoA (right). (D) Schematic summary highlighting the essential roles of myosins, AKMT and calcium signaling in controlling the apico-basal flux of F-actin. The events leading to parasite egress and motility are initiated by the activity of the cGMP-dependent protein kinase (PKG) which activates both the calcium and the lipid branches of the signaling pathway. APH, located on the microneme surface, binds to PA and mediates microneme exocytosis. CDPK1, activated by the calcium release, controls microneme secretion, F-actin apico-basal flux and conoid protrusion. CDPK1 possibly activates AKMT that is also essential for the flux. The exact molecular effectors of both enzymes are however not known. FRM1, localized at the apical end, generates the actin filament that will be further stabilized by GAC in complex with the secreted adhesins. The entire complex will then be translocated to the rear of the parasite, by the successive actions of MyoH and MyoA, generating forward motion.