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Home Journal Highlights New Insights into the Coat Shifting of Immune-Evading Trypanosomes
New Insights into the Coat Shifting of Immune-Evading Trypanosomes Print E-mail

 

African trypanosomes, spread by the tsetse fly, cause African sleeping sickness, and a related livestock disease, nagana. stannerudenkoSleeping sickness is fatal if untreated, but available medication is highly toxic. Trypanosomes multiply in the blood, evading immune attack by changing their dense, protective protein coats with frequency and regularly. These coats consist of variant surface glycoprotein (VSG). Hundreds of VSG genes exist, but only one can be expressed in an individual trypanosome's coat. Only one VSG expression site is active, while the rest are turned off. Back-to-back studies in the January Eukaryotic Cell, by Tara M. Stanne and Gloria Rudenko of the University of Oxford, United Kingdom, and by Luisa M. Figueiredo and George A. M. Cross of The Rockefeller University, New York, N.Y., show that the silent VSG expression sites are tightly wrapped in chromatin, while the active site is nearly naked, with few nucleosomes (a component of chromatin) compared to the silent sites. The implications: Chemicals that interfere with VSG expression site silencing have potential to be developed as drugs to treat this disease, says Rudenko. Figueiredo notes that this new understanding of how the active and silent VSG sites differ will help researchers design more productive experiments.

(T. M. Stanne and G. Rudenko. 2010. Active VSG expression sites in Trypanosoma brucei are depleted of nucleosomes. Eukaryot. Cell 9:136-147.)

(L. M. Figueiredo and G. A. M. Cross. 2010. Nucleosomes are depleted at the VSG expression site transcribed by RNA polymerase I in African trypanosomes. Eukaryot. Cell 9:148-154.)