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Nucleic Acids Research 2006 34(9):2710-2722; doi:10.1093/nar/gkl345
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Published online 19 May 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@oxfordjournals.org

Article

Modulation of telomere terminal structure by telomerase components in Candida albicans

Olga Steinberg-Neifach and Neal F. Lue*

Department of Microbiology and Immunology, W. R. Hearst Microbiology Research Center, Weill Medical College of Cornell University 1300 York Avenue, New York, NY 10021, USA

*To whom correspondence should be addressed. Tel: +1 212 746 6506; Fax: +1 212 746 8587; Email: nflue{at}med.cornell.edu

Received January 4, 2006. Revised February 7, 2006. Accepted April 18, 2006.

The telomerase ribonucleoprotein in Candida albicans is presumed to contain at least three Est proteins: CaEst1p, CaEst2p/TERT and CaEst3p. We constructed mutants missing each of the protein subunit of telomerase and analyzed overall telomere dynamics and single-stranded telomere overhangs over the course of many generations. The est1-{Delta}{Delta} mutant manifested abrupt telomere loss and recovery, consistent with heightened recombination. Both the est2-{Delta}{Delta} and est3-{Delta}{Delta} mutant exhibited progressive telomere loss, followed by the gradual emergence of survivors with long telomeres. In no case was telomere loss accompanied by severe growth defects, suggesting that cells with short telomeres can continue to proliferate. Furthermore, the amount of G-strand terminal overhangs was greatly increased in the est2-{Delta}{Delta} mutant, but not others. Our results suggest that in addition to their well-characterized function in telomere elongation, both CaEst1p and CaEst2p mediate some aspects of telomere protection in Candida, with the former suppressing excessive recombination, and the latter preventing excessive C-strand degradation.


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