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Nucleic Acids Research 2005 33(14):4536-4543; doi:10.1093/nar/gki769
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Published online 9 August 2005

© The Author 2005. Published by Oxford University Press. All rights reserved
The online version of this article has been published under an open access model. Users are entitled to use, reproduce, disseminate, or display the open access version of this article for non-commercial purposes provided that: the original authorship is properly and fully attributed; the Journal and Oxford University Press are attributed as the original place of publication with the correct citation details given; if an article is subsequently reproduced or disseminated not in its entirety but only in part or as a derivative work this must be clearly indicated. For commercial re-use, please contact journals.permissions{at}oupjournals.org

Article

Telomere structure and shortening in telomerase-deficient Trypanosoma brucei

Oliver Dreesen, Bibo Li and George A. M. Cross*

Laboratory of Molecular Parasitology, The Rockefeller University 1230 York Avenue, NY 10021-6399, USA

*To whom correspondence should be addressed. Tel: +1 212 327 7571; Fax: +1 212 3277845; Email: george.cross{at}rockefeller.edu

Received July 27, 2005. Accepted July 28, 2005.

Telomerase consists of a reverse transcriptase (TERT) and an RNA that contains a template for telomere-repeat extension. Telomerase is required to prevent telomere erosion and its activity or lack thereof is important for tumorigenesis and ageing. Telomerase has been identified in numerous organisms but it has not been studied in kinetoplastid protozoa. Trypanosoma brucei, the causative agent of African sleeping sickness, evades the host immune response by frequently changing its variant surface glycoprotein (VSG). The single expressed VSG is transcribed from one of ~20 subtelomeric ‘Expression Sites’, but the role telomeres might play in regulating VSG transcription and switching is unknown. We identified and sequenced the T.brucei TERT gene. Deleting TERT resulted in progressive telomere shortening of 3–6 bp per generation. In other organisms, the rate of telomere shortening is proportional to the length of the terminal 3' single-strand overhang. In T.brucei, G-overhangs were undetectable (<30 nt) by in-gel hybridization. The rate of telomere shortening therefore, agrees with the predicted shortening due to the end replication problem, and is consistent with our observation that G-overhangs are short. Trypanosomes whose telomere length can be manipulated provide a new tool to investigate the role of telomeres in antigenic variation.

GenBank accession no: AY904042


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O. Dreesen and G. A. M. Cross
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