Abstract
Toxoplasma gondii microneme is a specialized secretory organelle that discharges its contents at the apical tip of this apicomplexan parasite in a sequential and regulated manner. Increasing number of studies on microneme proteins (MICs) have shown them as a predominant and important role in host cell attachment, invasion, motility and pathogenesis. In this review, we summarize the research advances in one of the most important MICs complexes, TgMIC1/4/6, which will contribute to improve the understanding of the molecular mechanism of T. gondii infection and provide a theoretical basis for the effective control against T. gondii.
Highlights
Toxoplasma gondii is an obligate intracellular protozoan parasite of the phylum Apicomplexa with a unique apical complex composed of specialized cytoskeletal and secretory organelles, including rhoptries and micronemes
After TgMIC1/4/6 undergo conformation-dependent sorting and proteolytic processing events to obtain functional integrity, the regulation of their secretion becomes a necessary condition for the invasion of T. gondii into host cells, and the level of calcium ions in the parasites plays a key role in this process
It has been found that calcium-dependent protein kinase 1 (TgCDPK1) (Lourido et al, 2010, 2012; Lourido and Moreno, 2015; Brochet and Billker, 2016) and cyclic GMP activated protein kinase G (PKG) (Brown et al, 2017) which play a role in the downstream pathway of Ca2+, regulating the secretion of microneme proteins (MICs) until the end of invasion, and after that within the host cell, T. gondii endoplasmic reticulum (ER) uptakes Ca2+ to store via SERCA-type Ca2+ -ATPases, in order to use in the process of egress and the invasion (Figure 2; Billker et al, 2009; Lourido and Moreno, 2015)
Summary
Toxoplasma gondii is an obligate intracellular protozoan parasite of the phylum Apicomplexa with a unique apical complex composed of specialized cytoskeletal and secretory organelles, including rhoptries and micronemes. Rhomboid (ROM) 4, ROM5 and MPP1 hydrolyze the intramembrane region of the C-terminal transmembrane domain, so that the complex can be cleaved off the surface of T. gondii and disconnected from the host cell, resulting in an effective invasion.
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