In S. cerevisiae, mutations in genes that encode telomerase components, such as the genes EST1, ESM, EST3, and TLC1, result in the loss of telomerase activity in vivo [1-3], Two telemerase-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.
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