Abstract
Toxoplasma gondii possesses a limited set of actin-regulatory proteins and relies on only three formins (FRMs) to nucleate and polymerize actin. We combined filamentous actin (F-actin) chromobodies with gene disruption to assign specific populations of actin filaments to individual formins. FRM2 localizes to the apical juxtanuclear region and participates in apicoplast inheritance. Restricted to the residual body, FRM3 maintains the intravacuolar cell-cell communication. Conoidal FRM1 initiates a flux of F-actin crucial for motility, invasion and egress. This flux depends on myosins A and H and is controlled by phosphorylation via PKG (protein kinase G) and CDPK1 (calcium-dependent protein kinase 1) and by methylation via AKMT (apical lysine methyltransferase). This flux is independent of microneme secretion and persists in the absence of the glideosome-associated connector (GAC). This study offers a coherent model of the key players controlling actin polymerization, stressing the importance of well-timed post-translational modifications to power parasite motility.
Highlights
The large phylum of Apicomplexa is composed of thousands of protozoan pathogens of medical and veterinary significance including Toxoplasma gondii and the Plasmodium species responsible for toxoplasmosis and malaria, respectively (Adl et al, 2007; Seeber and Steinfelder, 2016)
FRM2 localizes to the apical juxtanuclear region and participates in apicoplast inheritance
In addition to a severe defect in apicoplast inheritance, myosin F (MyoF) deletion resulted in daughter cells growing in abnormal orientations and the formation of enlarged residual body (RB) filled with secretory organelles (Jacot et al, 2013)
Summary
The large phylum of Apicomplexa is composed of thousands of protozoan pathogens of medical and veterinary significance including Toxoplasma gondii and the Plasmodium species responsible for toxoplasmosis and malaria, respectively (Adl et al, 2007; Seeber and Steinfelder, 2016). In T. gondii, generation and dynamics of F-actin are known to be critical for apicoplast inheritance (Andenmatten et al, 2013; Jacot et al, 2013), constriction of the basal pole, intravacuolar cell-cell communication (Frenal et al, 2017b; Periz et al, 2017) and gliding motility (Dobrowolski and Sibley, 1996; Drewry and Sibley, 2015; Wetzel et al, 2003) (Figure 1A). The apicoplast segregates between the two forming daughter cells through the action of myosin F (MyoF), a motor conserved across the phylum of Apicomplexa (Jacot et al, 2013). Dense granules constitutively secrete dense-granules proteins (GRAs) both into and beyond the PV
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