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Molecular and Cellular Biology, July 2006, p. 4911-4919, Vol. 26, No. 13
0270-7306/06/$08.00+0     doi:10.1128/MCB.00212-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

Telomerase-Independent Stabilization of Short Telomeres in Trypanosoma brucei

Oliver Dreesen and George A. M. Cross*

Laboratory of Molecular Parasitology, The Rockefeller University, New York, New York 10021

Received 6 February 2006/ Returned for modification 24 March 2006/ Accepted 7 April 2006

In cancer cells and germ cells, shortening of chromosome ends is prevented by telomerase. Telomerase-deficient cells have a replicative life span, after which they enter senescence. Senescent cells can give rise to survivors that maintain chromosome ends through recombination-based amplification of telomeric or subtelomeric repeats. We found that in Trypanosoma brucei, critically short telomeres are stable in the absence of telomerase. Telomere stabilization ensured genomic integrity and could have implications for telomere maintenance in human telomerase-deficient cells. Cloning and sequencing revealed 7 to 27 TTAGGG repeats on stabilized telomeres and no changes in the subtelomeric region. Clones with short telomeres were used to study telomere elongation dynamics, which differed dramatically at transcriptionally active and silent telomeres, after restoration of telomerase. We propose that transcription makes the termini of short telomeres accessible for rapid elongation by telomerase and that telomere elongation in T. brucei is not regulated by a protein-counting mechanism. Many minichromosomes were lost after long-term culture in the absence of telomerase, which may reflect their different mitotic segregation properties.

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

Molecular and Cellular Biology, July 2006, p. 4911-4919, Vol. 26, No. 13
0270-7306/06/$08.00+0     doi:10.1128/MCB.00212-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Barnes, R. L., McCulloch, R. (2007). Trypanosoma brucei homologous recombination is dependent on substrate length and homology, though displays a differential dependence on mismatch repair as substrate length decreases. Nucleic Acids Res 35: 3478-3493 [Abstract] [Full Text]  
  • Glover, L., Alsford, S., Beattie, C., Horn, D. (2007). Deletion of a trypanosome telomere leads to loss of silencing and progressive loss of terminal DNA in the absence of cell cycle arrest. Nucleic Acids Res 35: 872-880 [Abstract] [Full Text]  
  • Dreesen, O., Cross, G. A. M. (2006). Consequences of Telomere Shortening at an Active VSG Expression Site in Telomerase-Deficient Trypanosoma brucei. Eukaryot Cell 5: 2114-2119 [Abstract] [Full Text]  


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