Essential nucleus-apical pole linkage maintains division fidelity during Plasmodium progeny formation.

Plasmodium parasites, the causative agents of malaria, undergo complex replication within vertebrate and insect hosts, presenting unique opportunities for therapeutic intervention. A key challenge during these replication events, i.e., schizogony in vertebrate red blood cells and sporogony in oocysts within mosquitos, is ensuring the faithful partitioning of nuclei and organelles into the numerous daughter cells that form at once from a single parental cell. While nuclear microtubule-organizing centers, or centriolar plaques (CPs), have been hypothesized to play a central role in this process, the molecular mediators linking CPs and organelles remain incompletely defined. Here, we characterize the roles of two striated fiber assemblin (SFA) homologs, SFA1 and SFA2, in replication of Plasmodium falciparum and Plasmodium berghei across two hosts. We show that these SFAs form a physical bridge between the CP and the nascent apical poles of daughter cells, facilitating high-fidelity progeny formation during schizogony and sporogony. Loss of SFA function disrupts merozoite and sporozoite formation, with profound consequences for transmission. These findings identify striated fiber assemblins as essential organizers of parasite morphogenesis and potential targets for anti-malarial therapies.