SGS1 is required for telomere elongation in the absence of telomerase

Abstract In 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.