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SGS1 is required for telomere elongation in the absence of telomerase

By Pei-Hsiu Huang, Fiona E. Pryde, Darren Lester, Rachelle L. Maddison, Rhona H. Borts, Ian D. Hickson and Edward J. Louis

Abstract

The full-text of this item is currently not available on the LRA. The original published version can be found on the publisher's website at: http://www.cell.com/current-biology/archive\ud doi:10.1016/S0960-9822(01)00021-5In S. cerevisiae, mutations in genes that encode telomerase components, such as the genes EST1, EST2, EST3, and TLC1, result in the loss of telomerase activity in vivo [1-3]. Two telomerase-independent mechanisms can overcome the resulting senescence. Type I survival is characterized by amplification of the subtelomeric Y' elements with a short telomere repeat tract at the terminus [4]. Type II survivors arise through the abrupt addition of long tracts of telomere repeats [4-6]. Both mechanisms are dependent on RAD52[4,5] and on either RAD50 or RAD51[6,7]. We show here that the telomere elongation pathway in yeast (type II) is dependent on SGS1, the yeast homolog of the gene products of Werner's (WRN) [8] and Bloom's (BLM) [9] syndromes. Survival in the absence of SGS1 and EST2 is dependent upon RAD52 and RAD51 but not RAD50. We propose that the RecQ family helicases are required for processing a DNA structure specific to eroding telomeres

Publisher: Elsevier (Cell Press)
Year: 2001
DOI identifier: 10.1016/S0960-9822(01)00021-5
OAI identifier: oai:lra.le.ac.uk:2381/8770
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