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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Abrupt disruption of capping and a single source for recombinationally elongated telomeres in Kluyveromyces lactis
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Abrupt disruption of capping and a single source for recombinationally elongated telomeres in Kluyveromyces lactis

机译：乳酸克鲁维酵母中的加盖端粒和重组延长端粒的单一来源突然中断

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摘要

Eukaryotic cells, including some human cancers, that lack telom-erase can sometimes maintain telomeres by using recombination. It was recently proposed that recombinational telomere elongation (RTE) in a telomerase-deletion mutant of the yeast Kluyveromyces lactis occurs through a roll-and-spread mechanism as described in our previous work. According to this model, a tiny circle of telomeric DNA is copied by a rolling-circle mechanism to generate one long telomere, the sequence of which is then spread to all other telomeres by gene-conversion events. In support of this model, we demonstrate here that RTE in K. lactis occurs by amplification of a sequence originating from a single telomere. When a mutationally tagged telomere is of normal length, its sequence is spread to all other telomeres at a frequency (≈10%) consistent with random selection among the 12 telomeres in the cell. However, when the mutationally tagged telomere is considerably longer than other telomeres, cellular senescence is partially suppressed, and the sequence of the tagged telomere is spread to all other telomeres in > 90% of cells. Strikingly, the transition between a state resistant to recombination and a state capable of initiating recombination is abrupt, typically occurring when telomeres are ≈3-4 repeats long. Last, we show that mutant repeats that are defective at regulating telomerase are also defective at regulating telomere length during RTE.
机译：缺少端粒擦除酶的真核细胞，包括某些人类癌症，有时可以通过重组来维持端粒。最近有人提出，乳酸克鲁维酵母的端粒酶缺失突变体中的重组端粒延伸（RTE）是通过我们以前的工作中描述的滚动和扩散机制发生的。根据该模型，端粒DNA的微小环通过滚环机制被复制以产生一个长端粒，然后其端粒通过基因转化事件传播到所有其他端粒。为了支持该模型，我们在此处证明乳酸克鲁维酵母中的RTE通过扩增源自单个端粒的序列而发生。当突变标记的端粒具有正常长度时，其序列以与细胞中12个端粒中随机选择一致的频率（≈10％）扩散到所有其他端粒。但是，当突变标记的端粒比其他端粒长得多时，细胞衰老会受到部分抑制，并且标记的端粒的序列会扩散到90％以上的细胞中的所有其他端粒。令人惊讶的是，在抗重组状态和能够启动重组状态之间的过渡突然发生，通常发生在端粒≈3-4重复长时。最后，我们显示在调控端粒酶方面存在缺陷的突变体重复序列在RTE期间在调控端粒长度方面也存在缺陷。

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