SGS1 is required for telomere elongation in the absence of telomerase
SGS1 is required for telomere elongation in the absence of telomerase
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DOI：
10.1016/s0960-9822(01)00021-5
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发表时间：
2001-01-23
期刊：
影响因子：
9.2
通讯作者：
Louis, EJ
中科院分区：
文献类型：
--
作者：
Huang, PH;Pryde, FE;Louis, EJ
In S.在酿酒酵母中，编码端粒酶组分的基因（例如基因EST 1、ESM、EST 3和TLC 1）中的突变导致体内端粒酶活性的丧失[1-3]。两种不依赖于端粒酶的机制可以克服所导致的衰老。I型存活的特征在于在末端具有短端粒重复序列的亚端粒Y '元件的扩增[4]，II型存活通过突然添加长端粒重复序列而产生[4-6]，两种机制都依赖于RAD 52 [4，5]以及RAD 50或RAD 51 [6，7]，我们在这里表明，酵母（II型）中的端粒延伸途径依赖于SGS 1，Werner（WRN）[8]和Bloom（BLM）[9]综合征基因产物的酵母同源物。在缺乏SGS 1和EST 2的情况下，生存依赖于RAD 52和RAD 51，但不依赖于RAD 50。我们提出，RecQ家族解旋酶是加工特异于侵蚀端粒的DNA结构所必需的。
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.