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Nucleic Acids Research 2006 34(1):96-103; doi:10.1093/nar/gkj417
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Published online 10 January 2006

© The Author 2006. 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}oxfordjournals.org

Article

High incidence of rapid telomere loss in telomerase-deficient Caenorhabditis elegans

Iris Cheung1,2, Michael Schertzer1, Ann Rose2 and Peter M. Lansdorp1,3,*

1Terry Fox Laboratory, BC Cancer Agency Avenue, Vancouver, BC, Canada V5Z 1L3 2Department of Medical Genetics, University of British Columbia Vancouver, BC, Canada V6T 1Z3 3Department of Medicine, University of British Columbia Vancouver, BC, Canada V5Z 4E3

*To whom correspondence should be addressed. Tel: +1 604 675 8135; Fax: +1 604 877 0712; Email: plansdor{at}bccrc.ca

Received September 20, 2005. Revised December 13, 2005. Accepted December 13, 2005.

Telomerase is essential to maintain telomere length in most eukaryotes. Other functions for telomerase have been proposed but molecular mechanisms remain unclear. We studied Caenorhabditis elegans with a mutation in the trt-1 telomerase reverse transcriptase gene. Mutant animals showed a progressive decrease in brood size and typically failed to reproduce after five generations. Using PCR analysis to measure the length of individual telomere repeat tracks on the left arm of chromosome V we observed that trt-1 mutants lost ~125bp of telomeric DNA per generation. Chromosome fusions involving complex recombination reactions were observed in late generations. Strikingly, trt-1 mutant animals displayed a high frequency of telomeres with many fewer repeats than average. Such outlying short telomeres were not observed in mrt-2 mutants displaying progressive telomere loss very similar to trt-1 mutants. We speculate that, apart from maintaining the average telomere length, telomerase is required to prevent or repair sporadic telomere truncations that are unrelated to the typical ‘end-replication’ problems.

Present address: Iris Cheung, Department of Molecular Biology, Princeton University, Princeton, NJ 08544, USA


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