Genomic Localization of TgSMC1 in Toxoplasma gondii parasites
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ABSTRACT: Apicomplexa are intracellular parasites that cause human and animal disease. They proliferate by a unique mechanism that combines closed mitosis with daughter cell budding. In past work we demonstrated that the Toxoplasma gondii centromeres are sequestered to the nuclear periphery proximal to the centrosome throughout the cell cycle. Here we show that interphase centromere clustering is not mediated by the mitotic spindle. Instead we propose a chromatin model of centromere clustering and define structural maintenance of chromosomes protein 1 (SMC1) as a persisting centromeric protein. We biochemically identify proteins that physically interact with SMC1, and CenH3 (a centromeric histone); prominent among those are predicted peripheral soluble components of the nuclear pore complex including TgExportin1. Treatment of parasites with the highly specific exportin1 inhibitor leptomycin B causes the dispersal of centromeres. Our results suggest that the nuclear envelope, and in particular peripheral components of the nuclear transport machinery orchestrate centromere positioning and parasite nuclear architecture.
ORGANISM(S): Toxoplasma gondii Toxoplasma gondii ME49
PROVIDER: GSE61806 | GEO | 2014/09/27
SECONDARY ACCESSION(S): PRJNA262179
REPOSITORIES: GEO
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