The glideosome-associated connector protein transitions between open and closed states, and this regulates its assembly and function during apicomplexan parasite motility.

The structure of full-length myosin A provides some hints about its atypical mechanism, and reveals that the light chain PfELC is a target to block malaria pathogenesis.

Toxoplasma gondii formins have several non-overlapping roles including generating an apico-basal flux of F-actin that is controlled by phosphorylation and methylation and is essential for motility.

A combination of high-resolution microscopy and reverse genetics identified key components of the alveolin network playing an essential role in the assembly of subpellicular microtubules and conoid in Toxoplasma gondii..

Parasites constrict as they propel themselves through the extracellular matrix one body length at a time, in a process highly reminiscent of host cell invasion.

A systemic proteome of the pellicle organelle inner membrane complex (IMC) provides new insight for the intraerythrocytic proliferation of malaria parasite and identifies the palmitoyl-acyl-transferase DHHC2 as a key enzyme regulating the localization of IMC proteins through palmitoylation.

This comprehensive transcriptomic resource of dormant and replicating malaria liver parasites highlights the dearth of pathways that operate in the hypnozoites and the need to investigate druggability (i.e. selectivity and safety) of core pathways in malaria parasites.

Time-resolved phosphoproteomics and thermal proteome profiling reveal the Ca²⁺-responsive proteome of the model apicomplexan Taxoplasma gondii, identifying PP1 as a Ca²⁺-responsive enzyme that regulates Ca²⁺ uptake to promote parasite motility.

Formin-2 controls spatiotemporal polymerisation of actin filaments, a common mechanism used by apicomplexans for effective segregation of essential chloroplast-like organelles called apicoplasts, and additionally for daughter formation in Plasmodium falciparum.

Analysis of chromerid algal genomes reveals how apicomplexans have evolved from free-living algae into successful eukaryotic parasites via massive losses and re-inventing functional roles of genes.