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Eukaryotic Cell, December 2006, p. 2114-2119, Vol. 5, No. 12
1535-9778/06/$08.00+0 doi:10.1128/EC.00059-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.
,
Laboratory of Molecular Parasitology, The Rockefeller University, New York, New York
Received 24 February 2006/ Accepted 16 October 2006
Trypanosoma brucei evades the host immune response by sequential expression of a large family of variant surface glycoproteins (VSG) from one of
20 subtelomeric expression sites (ES). VSG transcription is monoallelic, and little is known about the regulation of antigenic switching. To explore whether telomere length could affect antigenic switching, we created a telomerase-deficient cell line, in which telomeres shortened at a rate of 3 to 6 bp at each cell division. Upon reaching a critical length, short silent ES telomeres were stabilized by a telomerase-independent mechanism. The active ES telomere progressively shortened and frequently broke. Upon reaching a critical length, the short active ES telomere stabilized, but the transcribed VSG was gradually lost from the population and replaced by a new VSG through duplicative gene conversion. We propose a model in which subtelomeric-break-induced replication-mediated repair at a short ES telomere leads to duplicative gene conversion and expression of a new VSG.
Published ahead of print on 27 October 2006.
Supplemental material for this article may be found at http://ec.asm.org/.
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