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- W2118211168 abstract "The principal immune-evasion strategy of the extracellular protozoan parasite Trypanosoma brucei is one of antigenic variation (reviewed in [1–4]). In the mammalian host bloodstream, the parasite adopts a dense cell surface coat composed predominantly of a single immunogenic variable surface glycoprotein (VSG). Periodic switching of the expressed VSG gene results in successive changes in the antigenic identity of cells, prolonging parasitaemia and increasing probability of transmission. To this end, the organism maintains a population of around 100 small linear chromosomes which carry a library of divergent VSG genes at subtelomeric locations (see [5,6]). These minichromosomes (MCs) are between 30 and 150 kb in size and consist of a large palindromic core region made up of 177 bp tandem repeats (Wickstead et al., submitted for publication), subtelomeric VSG genes [7,8], canonical eukaryotic telomeres [9], and smaller portions of other repetitive DNAs (for example, 70 bp repeats [10]). They are also transcriptionally silent—minichromosomal VSG genes only become active upon duplicative transposition to active VSG expression sites (VSG-ESs) occurring on larger chromosomes. Central to the role of MCs in T. brucei is the diversity of VSG genes that they carry. A large diversity within the population of MCs can be maintained only if individual MCs are segregated with fidelity at mitosis—without mitotic fidelity, stochastic impetus will inevitably reduce the" @default.
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- W2118211168 date "2003-12-01" @default.
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- W2118211168 title "The mitotic stability of the minichromosomes of Trypanosoma brucei" @default.
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- W2118211168 doi "https://doi.org/10.1016/j.molbiopara.2003.08.007" @default.
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