Authors

D Soldati-Favre¹;  ¹ University of Geneva, Switzerland

Discussion

Toxoplasma gondii and other apicomplexans rely on gliding motility to traverse biological barriers, exit host cells, and initiate invasion, powered by the glideosome, a specialized actomyosin-based molecular machinery. Central to this process is the conoid, a dynamic organelle composed of tubulin fibers and preconoidal rings, where the glideosome assembles. These parasites also deploy a sophisticated arsenal of secretory organelles to breach and remodel host cells. T. gondii possesses 10–12 rhoptries that can repeatedly inject their contents into uninfected host cells, a virulence strategy known as iterative rhoptry discharge. This process depends on two short intraconoidal microtubules (ICMTs) within the conoid, decorated with vesicles that presumably replenish the apical vesicle, a central component of the rhoptry secretion machinery. The mechanisms by which ICMTs coordinate rhoptry deployment, however, remain largely unexplored. Recent advances in nanoscale imaging, proximity labeling, and post-translational profiling have begun to reveal how the conoid functions as a highly dynamic and regulated organellar system and serves as a gatekeeper for parasite motility. Comparative methylome analyses highlight lysine methylation as a conserved regulatory layer that modulates conoid dynamics, apical complex architecture, and glideosome assembly. Together, these findings illustrate how cytoskeletal organization, organelle positioning, and post-translational modifications converge to orchestrate parasite motility and host cell invasion in Apicomplexa.