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Toxoplasma gondii sequesters centromeres to a specific nuclear region throughout the cell cycle.


ABSTRACT: Members of the eukaryotic phylum Apicomplexa are the cause of important human diseases including malaria, toxoplasmosis, and cryptosporidiosis. These obligate intracellular parasites produce new invasive stages through a complex budding process. The budding cycle is remarkably flexible and can produce varied numbers of progeny to adapt to different host-cell niches. How this complex process is coordinated remains poorly understood. Using Toxoplasma gondii as a genetic model, we show that a key element to this coordination is the centrocone, a unique elaboration of the nuclear envelope that houses the mitotic spindle. Exploiting transgenic parasite lines expressing epitope-tagged centromeric H3 variant CenH3, we identify the centromeres of T. gondii chromosomes by hybridization of chromatin immunoprecipitations to genome-wide microarrays (ChIP-chip). We demonstrate that centromere attachment to the centrocone persists throughout the parasite cell cycle and that centromeres localize to a single apical region within the nucleus. Centromere sequestration provides a mechanism for the organization of the Toxoplasma nucleus and the maintenance of genome integrity.

SUBMITTER: Brooks CF 

PROVIDER: S-EPMC3048097 | biostudies-literature | 2011 Mar

REPOSITORIES: biostudies-literature

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Toxoplasma gondii sequesters centromeres to a specific nuclear region throughout the cell cycle.

Brooks Carrie F CF   Francia Maria E ME   Gissot Mathieu M   Croken Matthew M MM   Kim Kami K   Striepen Boris B  

Proceedings of the National Academy of Sciences of the United States of America 20110214 9


Members of the eukaryotic phylum Apicomplexa are the cause of important human diseases including malaria, toxoplasmosis, and cryptosporidiosis. These obligate intracellular parasites produce new invasive stages through a complex budding process. The budding cycle is remarkably flexible and can produce varied numbers of progeny to adapt to different host-cell niches. How this complex process is coordinated remains poorly understood. Using Toxoplasma gondii as a genetic model, we show that a key e  ...[more]

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