Telomerase-independent lengthening of yeast telomeres occurs by an abrupt Rad50p-dependent, Rif-inhibited recombinational process.
Telomerase-independent lengthening of yeast telomeres occurs by an abrupt Rad50p-dependent, Rif-inhibited recombinational process.
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DOI：
10.1016/s1097-2765(05)00094-8
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发表时间：
2000-10
期刊：
影响因子：
16
通讯作者：
S. Teng;Jason Chang;Bradley McCowan;V. Zakian
中科院分区：
文献类型：
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作者：
S. Teng;Jason Chang;Bradley McCowan;V. Zakian
II型幸存者出现在缺乏端粒酶的酵母细胞中，通过重组途径导致非常长和不同长度的端粒。在这里，我们展示了II型端粒突然出现在端粒非常短的细胞群体中。一旦建立，这些长的端粒就会逐渐缩短。短的端粒是罕见的一步延长事件的底物。II型幸存者的世代绝对依赖于Rad50p。在端粒酶熟练的细胞中，端粒结合的Rif蛋白抑制了端粒的端粒酶延长。在端粒酶缺乏的菌株中，Rif蛋白，特别是Rif2p，抑制了II型重组。这些数据认为，只有较短的端粒是II型重组的底物，并表明这种重组的供体不是染色体端粒。
Type II survivors arise inSaccharomycescells lacking telomerase by a recombinational pathway that results in very long and heterogeneous length telomeres. Here we show that type II telomeres appeared abruptly in a population of cells with very short telomeres. Once established, these long telomeres progressively shortened. Short telomeres were substrates for rare, one-step lengthening events. The generation of type II survivors was absolutely Rad50p dependent. In a telomerase-proficient cell, the telomere-binding Rif proteins inhibited telomerase lengthening of telomeres. In a telomerase-deficient strain, Rif proteins, especially Rif2p, inhibited type II recombination. These data argue that only short telomeres are substrates for type II recombination and suggest that the donor for this recombination is not a chromosomal telomere.