This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Supplemental material
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowReprints and Permissions
Right arrow Copyright Information
Right arrow Books from ASM Press
Right arrow MicrobeWorld
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Dreesen, O.
Right arrow Articles by Cross, G. A. M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Dreesen, O.
Right arrow Articles by Cross, G. A. M.

 Previous Article  |  Next Article 

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.

Consequences of Telomere Shortening at an Active VSG Expression Site in Telomerase-Deficient Trypanosoma brucei{triangledown} ,{dagger}

Oliver Dreesen and George A. M. Cross*

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.

* Corresponding author. Mailing address: Laboratory of Molecular Parasitology, The Rockefeller University, 1230 York Avenue, New York, NY 10021-6307. Phone: (212) 327-7571. Fax: (212) 327-7845. E-mail: george.cross{at}rockefeller.edu.

{triangledown} Published ahead of print on 27 October 2006.

{dagger} Supplemental material for this article may be found at http://ec.asm.org/.

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.





Copyright © 2009 by the American Society for Microbiology.   For an alternate route to Journals.ASM.org, visit: http://intl-journals.asm.org | More Info»