In S. cerevisiae, mutations in genes that encode telomerase components, suc
h 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 el
ongation 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 RAD5
1 but not RAD50, We propose that the RecQ family helicases are required for
processing a DNA structure specific to eroding telomeres.