Transmembrane proteins mediate basal complex assembly and individual daughter cell formation in malaria parasites.

Abstract

Asexual reproduction of malaria parasites requires the basal complex, the equivalent of a eukaryotic contractile ring. Despite its central role, basal complex biogenesis remains largely unknown. Here, we use expansion microscopy and DNA points accumulation for imaging in nanoscale topography to investigate three transmembrane basal complex proteins in <i>Plasmodium falciparum</i>-basal complex transmembrane protein 1 (BTP1), BTP2, and basolateral expansion boundary (BLEB). Parasites lacking BTP2 are still enveloped by membranes but fail to separate from each other, resulting in multiorganellar mutants. We isolate the defect to a specific step during basal complex development and demonstrate that the contractile ability remains intact. By revisiting BLEB, we identify a distinct plasma membrane region that is excluded from daughter cells and associated with the basal complex. Integrating these findings, we propose a three-step model for basal complex biogenesis that highlights the specific role of BTP2 and suggests a role for the BLEB-associated membrane. This study offers a mechanistic framework for how multiple daughter cells are formed simultaneously and highlights the importance of transmembrane proteins for cell division.