Abstract

The African trypanosomes, which are the causal agents of African Sleeping Sickness in humans, undergo in the bloodstream of the mammalian host a selective expression of variant surface glycoprotein (VSG) genes as a mechanism to evade the immune response of the host (5). The trypanosomes have up to 20 different telomeric-localized expression sites and more than a hundred VSG genes, and are able to modulate VSG expression by several mechanisms, including replacing the VSG gene in the active expression site or activating a new expression site and silencing the old site (6). The mechanism for silencing all but one VSG sites and for the inheritance of these stable transcriptional states is unknown but is thought to involve an epigenetic mechanism because it is independent of promoter sequences. The original discovery of J stemmed from the observation that silenced telomeric genes could not be digested with restriction enzymes …

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