Received: Accepted: JPublished: August 22, 2022Ĭopyright: © 2022 Munera Lopez et al. PLoS Pathog 18(8):Įditor: Isabelle Coppens, Johns Hopkins University Bloomberg School of Public Health, UNITED STATES (2022) An apical protein, Pcr2, is required for persistent movement by the human parasite Toxoplasma gondii. The discovery of Pcr2 and the analysis of its function open new opportunities to determine how mechanical interactions with its environment impact parasite motility, and how the regulation or maintenance of persistence in parasite movement is functionally connected with and imposed onto the motility apparatus and other structures involved in invasion and egress.Ĭitation: Munera Lopez J, Tengganu IF, Liu J, Murray JM, Arias Padilla LF, Zhang Y, et al. Furthermore, the ability of the Pcr2 knockout parasite to assemble a ring-like structure (the moving junction) at the entry point of invasion, is impaired. As a result, Pcr2 knockout parasites cause much less host tissue destruction. The movement of the Pcr2 knockout parasite is spasmodic, which compromises egress and invasion, two vital steps in the parasite’s lytic cycle. We discovered that Preconoidal region protein 2 (Pcr2), a new component of the parasite apical complex, is important for the persistence of Toxoplasma movement. Here we investigate the movement of a very successful apicomplexan, Toxoplasma gondii. Cell movement, needed to disseminate among tissues and invade into a host cell, is essential for the apicomplexan parasites to maintain their intracellular parasitic life style. The thousands of species of apicomplexan parasites are responsible for many devastating human and animal diseases, including malaria and toxoplasmosis. Interestingly, actomyosin activity, as indicated by the motion of mEmerald tagged actin chromobody, appears to be largely unperturbed by the loss of Pcr2, raising the possibility that Pcr2 may act downstream of or in parallel with the actomyosin machinery. Both defects likely contribute to the poor efficiency of invasion. In addition to faulty motility, the ability of the Pcr2 knockout parasite to assemble the moving junction is impaired. However, the movement of the Pcr2 knockout parasite is spasmodic, which drastically compromises egress. Calcium-induced secretion of the major adhesin, MIC2, also appears to be normal. When stimulated for calcium-induced egress, Pcr2 knockout parasites become active, and secrete effectors to lyse the host cell. Pcr2 knockout parasites replicate normally, but they are severely diminished in their capacity for host tissue destruction due to significantly impaired invasion and egress, two vital steps in the lytic cycle. Here we report the identification and characterization of a new component of the apical complex, Preconoidal region protein 2 (Pcr2). During invasion, the parasite first makes contact with the host cell "head-on" with the apical complex, which features an elaborate cytoskeletal apparatus and associated structures. One of the most effective invaders in Apicomplexa is Toxoplasma gondii, which can infect any nucleated cell and any warm-blooded animal. The parasite moves by gliding on a surface, propelled by an internal cortical actomyosin-based motility apparatus. To infect, the parasite must first initiate active movement to disseminate through tissue and invade into a host cell, and then cease moving once inside. The phylum Apicomplexa includes thousands of species of unicellular parasites that cause a wide range of human and animal diseases such as malaria and toxoplasmosis.
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