The fission yeast Taz1 protein protects chromosomes from Ku-dependent end-to-end fusions
The fission yeast Taz1 protein protects chromosomes from Ku-dependent end-to-end fusions
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DOI：
10.1016/s1097-2765(01)00154-x
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发表时间：
2001-01-01
期刊：
影响因子：
16
通讯作者：
Cooper, JP
中科院分区：
文献类型：
--
作者：
Ferreira, MG;Cooper, JP
端粒最重要的作用是防止染色体融合。裂变酵母Taz1蛋白调节多种端粒功能，但对无胁迫条件下的生长不是必需的。然而，引人注目的是，taz1（-）细胞在遭受氮饥饿时表现出致命的端粒融合，这是一种诱导未确定G1状态的处理。这些融合是由依赖于ku的非同源末端连接形成的。在缺乏rad22（+）基因的taz1（-）细胞的正常生长过程中也会发生融合，rad22（+）基因参与同源重组。我们的数据提出了一个模型，其中taz1（-）端粒暴露于DNA修复的普遍模式，这是由细胞周期决定的。因此，Taz1覆盖染色体末端，并提供端粒特异性相互作用，阻止Ku将端粒视为双链断裂。
A paramount role of telomeres is to prevent chromosome fusions. The fission yeast Taz1 protein regulates diverse telomere functions but is not essential for growth under stress-free conditions. Strikingly, however, taz1(-) cells exhibit lethal telomere fusions when subjected to nitrogen starvation, a treatment that induces an uncommitted G1 state. These fusions are formed by Ku-dependent nonhomologous end joining. Fusions also occur during normal growth in taz1(-) cells that lack rad22(+), a gene involved in homologous recombination. Our data suggest a model whereby taz1(-) telomeres are exposed to the prevailing mode of DNA repair, which is dictated by the cell cycle. Thus, Taz1 caps chromosome ends and provides the telomere-specific interaction that prevents Ku from treating telomeres as double-strand breaks.