Formin-2 drives intracellular polymerisation of actin filaments enabling correct segregation of apicoplasts in Plasmodium falciparum and Toxoplasma gondii.

摘要: Pathogenic obligate-intracellular apicomplexan parasites possess an essential chloroplast-like organelle called the apicoplast that undergoes division and segregation during replication. Parasite actin is intracellular development, implicated in vesicular transport, parasite replication inheritance. However, inability to visualise live dynamics limited functional characterisation of both filamentous-actin (F-actin) regulatory factors. Apicomplexans at least two distinct formins, Formin-1 Formin-2, predicted serve as actin-nucleating factors, previously regulating gliding motility host cell invasion. Here, we expressed chromobodies validated them F-actin-binding sensors Plasmodium falciparum characterised vivo F-actin network. The network could be modulated chemically disrupted by conditionally deleting actin-1 gene. In a comparative approach, demonstrate Formin-2 closely associated with apicoplasts P. Toxoplasma gondii. Consequently, disruption resulted not only defect, but also complete abrogation parasites. Together, our results strongly indicate Formin-2-mediated filament formation common primary mechanism for nucleation growth effecting segregation.