Abstract
Apicomplexa are obligate intracellular parasites which cause various animal and human diseases including malaria, toxoplasmosis, and cryptosporidiosis. They proliferate by a unique mechanism that combines physically separated semi-closed mitosis of the nucleus and assembly of daughter cells by internal budding. Mitosis occurs in the presence of a nuclear envelope and with little appreciable chromatin condensation. A long standing question in the field has been how parasites keep track of their uncondensed chromatin chromosomes throughout their development, and hence secure proper chromosome segregation during division. Past work demonstrated that the centromeres, the region of kinetochore assembly at chromosomes, of Toxoplasma gondii remain clustered at a defined region of the nuclear periphery proximal to the main microtubule organizing center of the cell, the centrosome. We have proposed that this mechanism is likely involved in the process. Here we set out to identify underlying molecular players involved in centromere clustering. Through pharmacological treatment and structural analysis we show that centromere clustering is not mediated by persistent microtubules of the mitotic spindle. We identify the chromatin binding factor a homolog of structural maintenance of chromosomes 1 (SMC1). Additionally, we show that both TgSMC1, and a centromeric histone, interact with TgExportin1, a predicted soluble component of the nuclear pore complex. Our results suggest that the nuclear envelope, and in particular the nuclear pore complex may play a role in positioning centromeres in T. gondii.
Highlights
Apicomplexa are obligate intracellular parasites that cause various animal and human diseases including malaria, toxoplasmosis, and cryptosporidiosis
To investigate the mechanism mediating centromere clustering in T. gondii we propose to test two alternative hypotheses
Interphase as well as dividing parasites treated with oryzalin exhibit continued clustered localization for TgCenH3 (Figures 1B,C). These results suggested that the mitotic spindle is likely not responsible for centromere clustering during interphase
Summary
Apicomplexa are obligate intracellular parasites that cause various animal and human diseases including malaria, toxoplasmosis, and cryptosporidiosis. Apicomplexan parasites replicate by modes of division that differ from those used by their hosts (Francia and Striepen, 2014). Mammalian cells divide their nucleus by open mitosis in which the nuclear envelope breaks down, giving way to the mitotic spindle, and is immediately followed by cytokinesis (with few exceptions). Many structural and regulatory aspects of apicomplexan cell division are not wellunderstood (White and Suvorova, 2018)
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